Okay well we'll give you a chance after Dr. Bennett's talk to ask questions of everybody. So now I get to introduce C. Frank Bennett, otherwise we call him Frank. He's a great guy. He is an interesting fellow. He has worked at a drug company since 1989, IONUS, and his focus has been on how can we use these anti-sense molecules to attack disease. And in fact, Frank was I think helped in many ways by not only the HDF's activities, but many other researchers' activities, but together with collaboration it was possible to actually show that they could affect things in animals. Now the other thing that's really important that I just wanted to tell you about is Frank just won the breakthrough prize. Now the breakthrough prize, many people think it's well it's definitely better than the Nobel Prize because it's three million dollars, but also because it really is defining people doing just cutting-edge work and he did not get it for the work on Huntington's. He got it for the work on spinomuscular atrophy, a horrible disease where children are born and start to become weak either as infants or young children and they lose the neurons going to their muscles and just become weaker and weaker until they can't walk, they can't speak, they are eventually die at about the age of three or four or five. It's fatal disease. He designed an ASO, anti-sense oligonucleotide that worked and there are now kids running around with that disease at six, seven, eight. He'll tell, he could tell you after his talk about Huntington's about this. It is a miracle and it shows that if this can work in spinomuscular atrophy, it's going to work in other diseases and he's already trying it. So that's what's so exciting and he is so awesome because he gives of his time to really work out how we're going to get this done for diseases that aren't maybe the most common disease in the world but the diseases that are extremely important to many people. So, Frank, please. Maybe we have to stop there. So, thank you very much. That's very kind and I do appreciate being invited to speak here today. It's very, a lot of fun to talk about some of the work that we've been doing and now we're starting to see some of the benefit of that work come to fruition and also I should acknowledge that when Nancy asks you to do something, she's the godmother and you never say no to Nancy. So it's a pleasure to be here. And so what I'd like to do is go into a little bit more detail about some of the technology that Dr. Tillman just spoke about and just to remind you that our genes and there's roughly 20,000 to 25,000 unique genes in the human genome are made into an intermediate molecule called RNA and one way to think about this is the genes, the hard drive of your computer where all this information is stored, it's transcribed into an intermediate molecule called RNA that goes away over time so it doesn't hang around very long and then that RNA is translated into proteins which are the scaffolds and the enzymes and what make our body function. And so this has been referred to as the central dogma of life is that DNA makes RNA makes protein and fortunately some of the proteins that are made are toxic and will cause a disease. They can either be genetically caused proteins such as Huntington that produce toxicity or sometimes the cell makes modifications on proteins that cause them to be toxic. And so as an industry and I've been working in the pharmaceutical industry now for 35 years our goal is really trying to identify drugs that will interact with proteins and there's really two classes of drugs that we have traditionally thought about. One that moved a little bit but small molecules that will bind protein and these are drugs like Lipitor, Asperin, we all take a number of different small molecule drugs that do bind to protein and impact the protein and we'll, sorry, go back one, will bind to the protein and modify the disease. There's another class of proteins that's really coming to the forefront now called antibodies and these are protein drugs themselves that bind to proteins and we all have antibodies that we generate but you can design antibodies to bind to proteins that will interfere with their function and that's commonly used now in cancer therapy. In fact, a lot of the big excitement in cancer right now is because of the antibody-based therapies. They've been used for inflammatory diseases like rheumatoid arthritis, the TNF inhibitors that you may have heard about are examples of this and so that's really a powerful technology for modulating disease-causing proteins in the body. We as a company are taking a little bit different strategy and what we're doing is to design oligonucleotides or drugs that will bind to RNA and remember there's 20 to 25,000 unique genes in the genome. We can design an antisense drug shown here that will only bind to one of those so we're only binding to one of the 20,000 genes so it's a very selective way of modulating function. Once the oligonucleotide binds to this RNA here, it brings in an enzyme that causes it RNA to be degraded and the net result is you don't produce the protein. So we're a little bit upstream of what most traditional drugs do and that we're not binding to the protein itself but what we're doing is preventing the protein from ever being made. So by reducing the amount of RNA, you reduce the amount of toxic protein that's being produced in the cell. And that's really the basis for the technology that we're working on. That may sound very Star Warsy and it probably does is that how in the world can you make all this work? And I can show you that we've been able to make it work. There are currently six approved drugs that use this technology today and they range from a drug to treat a viral infection that was very prevalent during the AIDS epidemic, a drug for cholesterol, the spinal muscular atrophy drug that Anne just mentioned a few minutes ago and I'll talk more about. And then a drug for another very severe pediatric disease called the Schoen's muscular dystrophy that's being used and then recently two new drugs have come on the market for targeting polyneuropathy. So it's a peripheral nerve disorder that antisense drugs are really showing a lot of promise for. And so what I'd like to do is just for a moment show you Spinrasa because I think it has a lot of relevance to Huntington's disease and Spinrasa is a drug that was approved about a year and a half ago by the FDA for cell in the United States. And so as Anne mentioned, SMA is what's called a motor neuron disease. So the nerves that innervate your muscle become sick. And one way I kind of use as an analogy is if you think about an electric cord being plugged into an outlet, those are your nerves being plugged into the muscle. And when these nerves get sick, they sort of fall out of the socket. So the nerve hasn't completely died off, but it's not making the electrical connection, so you're not firing the muscle. And eventually these kids will become paralyzed. So the disease presents as a spectrum, the most severe form of the disease is called type one SMA. And these are infants that generally present symptoms within one to two months of life. They start losing their muscle function. And unfortunately, they have a very short life expectancy of six months to a couple of years. And historically have been called the floppy infant syndrome today. There's another less severe form of the disease called type two SMA where they develop symptoms after six months of age and they're able to sit. So they do have some function and they'll live to their 20s and longer. But they are severely impacted by the disease. They have very severe contractures. They lose weight and don't have a high quality of life. But they do have a fairly normal life expectancy. And then there's the type three kids who again have the ability to walk. But as they start going through puberty and putting on a lot of weight, they stress out their muscles and they end up losing muscle tone. And so they lose the ability to walk later in life. And it really is a continuum. It doesn't really fit into a specific category. But it sort of gives you the extremes of what we're looking at. Unfortunately, these type one infants account for about 50% of the babies born will have this type one SMA. So that's the most severe form. And unfortunately, it's the most common today. So as mentioned, we developed a drug for type one SMA. And what I'd like to do, rather than show you a lot of numbers and graphs showing the activity of the drug, is actually show you a patient that was treated. And so this is Cameron, just to introduce you, who is a type one SMA baby. He was diagnosed about seven weeks of age and went on the drug at eight weeks of age. And so what I'd like to do is show you his progression while on the drug. And so if you could start the video. So this is four weeks old and looks like a relatively normal healthy baby, although he's not showing a lot of movement in his arms there. By seven weeks, he's clearly symptomatic. He can barely move his hands. And then we started on drug and so by four and a half months, so it's a couple months after starting treatment, he's beginning to show some strength in his arms. And you'll you'll see, you know, at 12 months, a little bit more strength, getting better. Sorry. And then this shows him at 16 months. So he's beginning to get some strength in his legs. And you'll notice that he's kids really don't have any neck control, your head's pretty heavy for most of us.  By 20 months, he's beginning to stand. And this shows a picture at 26 months, a riding a horse. And by 36 months, he's riding a tricycle. So it really does show what this drug is done. And so just to remind you, this was what was anticipated that he would have become that really he would have been completely paralyzed by the time he's three years of age. And what we've done with treatment is I don't want to see we've converted them to a type two a less severe form of the disease, but it clearly resembles a lot of the symptoms of a type two SMA. And this should point out that he's still on therapy. And you can Google camera and SMA and you'll see the family post videos of their their child fairly frequently. He's now beginning to walk there. So really, we really don't know what what he's going to turn into and what the the future is in store for him. But it was much better than what the future was before this drug. And so that's why I'm personally excited about what we're doing in neurological disease is that I really do believe that we can have other examples like a spin rasa that we're going to have an impact on a very severe neurodegenerative disease. And so what I'd like to do and given the audience is tomer attention to Huntington's disease. And just to remind you, Huntington's, as a Dr. Tillman pointed out, is a disease where there's an expansion of the CAG repeat within the genome to produce this toxic protein. And generally, the way to think about is the toxic protein becomes sticky. And so you get these large aggregates that bind and stick together and they gum up the cell and the cell can't really deal with them very well. And they end up becoming toxic to the cell. And so I do think it's worth noting today. This is the 50th anniversary of the hereditary disease foundation. It's the 25 year anniversary since the discovery of the gene. And many of the people in this room, there are several scientists in this room that were instrumental in the discovery of the gene, including Dr. Wexler. And this is a large group of people. And one of the things that's really astounding is now that we have the human genome sequence, this took over 50 people 10 years or so to be able to identify this gene. Today, scientists are discovering genes that cause disease every day. And just with the expansion of the sequencing information that's out there, it's very common to pick up a journal or a science article about new causes of diseases. And it's a really testament to this setting the foundation for how we go about discovering genes. So just to take a step back, and I wanted to spend just a couple minutes to talk about the how we develop drugs. And so most of you are aware that the first step in this process really heavily relies on the basic research that's being done to identify targets and then understand the biology of those targets. So you have proteins like Huntington that was discovered 25 years ago. And we're learning a lot about the protein, but there's still a lot of mysteries and a lot more information that's needed to be found. But it gives us a drug target because we know the protein causes the disease. So the thought is if we can lower the protein that should have an impact on the disease. Once we identify a target, the next step is what we call preclinical testing where we'll screen for drugs that will bind or modulate the protein or RNA of interest and test those in cell culture and animals. And then once we get some confidence that the drug is doing what it should be doing, we'll advance those into clinical trials. And just wanted to highlight that there is a little bit more complicated than just going into clinical trials is there's actually three different phases of clinical trials. Phase one is generally the first in human trial. And the primary focus is on safety. So we're really just looking to see is the drug safe to administer to patients. You really aren't dosing long enough to see any kind of clinical effect, but it is where you have to start before you can run. A phase two study has a larger number of patients. And this is where you begin to start looking for signs of efficacy. It's still safety is the primary focus, but you are looking for signs of efficacy. And then phase three is the large studies. Generally, there are hundreds of patients, if not thousands, depending on the drug that you're testing it in. And that's where you really do focus is the drug doing what it should be doing to treat a disease. So it is, unfortunately, a fairly long process that this can take anywhere from, in the case of Spinraza that I just showed, that was a five year from here to getting the drug approved. Most drugs, that's actually a fairly accelerated timeline. Most drugs are five to 10 years and sometimes even longer. So this takes some oil to be able to get the final approval of a drug. And the reason I point that out is I want to put in perspective where we are in the process. So when we first started working on the Huntington, it was actually a project that we were working on with Don Cleveland and CHDI was a key funder of the work that we were doing. And the goal was really trying to figure out strategy. How do we use our technology to be able to target the Huntington gene? And so we had a number of different discussions and one of the strategies was to design an anti-synth drug that would bind to the Huntington RNA as well as the wild type Huntington RNA and bring in this enzyme that would end up degrading the RNA. And we call that total Huntington ASO and that it reduces both the wild type and the mutant Huntington there. Another strategy that we've been looking at is that we have heterogeneity in our genome. So even though we all have the same genes, there's subtle differences, generally one or two nucleotide differences between my gene and your genes out there. And with our technology, we can actually exploit that difference and we can recognize a single nucleotide change between this gene and this gene. And so we can design an anti-synth drug that would bind to the mutant Huntington but not the wild type and that was very attractive to us that we can cause cleavage of the mutant Huntington allele or RNA that's produced off that but not the wild type and sort of leave the normal amount of Huntington protein intact. The problem is that this would only treat about 40% of the patients out there with one drug and we could develop a second drug that would treat another 20 to 30% of the patients and another drug that would treat 10%. And before you know it, we'd have to develop eight or nine drugs to be able to treat all the Huntington patients in the world. Whereas this strategy allows us to treat all the Huntington patients throughout the world with a single drug. And so ultimately after a lot of discussion with our partners Roche on this as well as internally, we opted to go with this strategy as a strategy to take into clinical trials. And doing that, we found that there was really no difference in the activity that we saw in mouse models and there are a number of different mouse models of Huntington that I don't really want to get into. This is just one example of a mouse model. And what you notice is that if we started treating here with the antisense drug, the mice actually started getting better. We didn't just stop the disease but we improved symptoms. And again, you have to put this in perspective. It is a mouse model, it's not the human disease. But it was encouraging that the mice were getting better with treatment. And just to kind of highlight what this is, it's called a rotorod test, which if you can imagine, it's a log rolling contest for mice. And you're actually measuring how long mice can stand up on the log.  And so it's commonly used in research, how long we do this. Actually, the researchers ought to have to do this as well to be able to administer the test. But it is, just think of it as the log rolling contest. And so you see that these mice are able to stay on the log a little bit longer than untreated mice with treatment. So that was very encouraging. And there were a number of other studies that we did that ultimately led us to start a clinical study. So what I'll share is just a little bit of the data from that first clinical study that we've done. This is, and I should have highlighted, these are all injectable drugs. So they have to use a needle. And in the case of Huntington, we're administering the drug into the cerebral spinal fluid that surrounds the brain at the base of the back. So it's basically a spinal tap. And I know that sounds horrible, but it's very commonly used and well tolerated by the patients that were in this study. And so the patients were given four doses of the drug. And it was called a dose escalation study. So the first group of patients were given 10 milligrams of drug. And there were about four patients that got that dose. We monitored them very carefully looking for any safety signals. And again, this is first time that we're ever exposing an experimental therapy to patients. So they're monitored for another four months after the dose was done. And look, make sure the drug was safe. Then the next group of patients got 30, the next group 60, the next 90, and 120. So it's a dose escalation study. It should point out that prior to dosing, because you are like you do have the needle in the cerebral spinal fluid, you collect a little bit of that fluid. And we use it for two things. One is that we measure safety to make sure there's no safety signals that are occurring that we can detect in cerebral spinal fluid. But importantly, as you'll see in the next slide, we're using it to document that the drug is doing what it should be doing. That is it's reducing the mutant huntington protein in CSF fluid, which reflects the mutant huntington protein in the brain. And so what we've demonstrated is a dose dependent reduction. So with the higher doses, we're seeing a lowering of the mutant huntington protein. Each dot represents an individual patient. And it shows the percent reduction that we see with the patients. And typical with the clinical trial, there is heterogeneity. Not everybody responds the same way to this drug, just like nobody responds to many other drugs. But if you look at the average, it was very encouraging that we were seeing this dose dependent reduction. Furthermore, we saw time dependent reduction. So first dose, second dose, third dose, you see it starting to go down more and more. We expect this to plateau off after four to five doses. So it's not going to just keep going down to zero, but it should show more robust reductions in the huntington protein than what we see today. And so what we're predicting, based upon a lot of modeling, is that a 40% reduction, which is here, would cause a 50 to 75% reduction in brain tissue. And so that's within the therapeutic range that we were seeing in the mouse models to produce the benefit that we saw in the mice. So we think we have a dose that should be effective at this point. So just as I said, this primary focus of the study was safety. And there were really no safety signals in the study. The drug was very well tolerated at all the doses. And none of the participants discontinued from the study. And in fact, we now have what's called an open label extension study. So all the patients who participated in the study were asked if they wanted to continue to receive the drug. And so they had to reenroll in a new study where they're getting the drug at the highest dose tested. And all 46 patients did reenroll. So they are, you know, further evidence that there were no side effects that would keep people out of participating in the study like this. And as I mentioned, this is a relatively short-term study. And so we never expected to see any kind of improvement in their symptoms at this stage. And we didn't. And so the thought is that you're going to have to treat for a longer period of time to really see improvements in symptoms of the patients. And so that brings me to what's next for this drug. You know, first off our partners Roche licensed the drug and, you know, supported doing the extension study. And they're about ready to launch a phase 3 study for this drug. So they're skipping phase 2. They want to accelerate getting this drug to patients as quickly as possible. And given the data that we had based upon the safety and the fact that we were engaging the target, that is that we were, the drug was doing what it should be doing. They're really starting a phase 3 study. And it has a, like all phase 3 studies, a fancy acronym called Generation HD that came out of this word. They pay people a lot of money to do this, I should say. But anyway, we're very excited to the study starting. And it is a fairly large study, 660 participants with 80 to 90 sites total in 15 countries throughout the world. So it will be a very big study. There are three arms to the study where patients will get 120 milligrams of the drug monthly, 120 milligrams every other month, or the placebo monthly. And it will, all the patients who finish the study will then have the option of enrolling into an open label study where they will all get drug, even the placebo patients will get the drug. As long as the drug is safe and no safety signals show up. So really, I just wanted to leave it here, I think, is that this is not the end. This is Winston Churchill's quote, I should mention, not mine. But really, we're at the beginning of the, it's the end of the beginning is where we are. So there's still a lot more work to be done. And just to kind of highlight and that Dr. Tillman talked about this, is that, you know, we feel that INS-HDTRX, which has now got a Rosh number, RG604, or for two, offers hope that Huntington may be a treatable disease. We haven't proven it yet, and so we still have to do that. It's important, because this is still very early, that we continue to invest in developing other therapies.  In fact, I'd be astonished that we actually cure the disease. So it really is to be thought of as a treatment. And to make the treatments more effective, it's important to keep investing in alternative treatments to go forward. And to do that, we need to find additional drug targets. And Dr. Tillman already talked about some of the modifier genes that have been identified, that HDF has been instrumental in helping to mine to get those. And ultimately, our goal is to continue with basic research to find additional targets, as well as clinical and translational research. We need to do both. And so with that, I'll skip this, because Dr. Tillman already talked about it. But I just wanted to thank the investigators who participated in the clinical trial. It was led by last year's honoree for the award, Dr. Sarah Tabrizzi. And you may have heard her talk last year. She's much more dynamic than I am. Sorry. And then finally, my collaborators that were really instrumental at UCSD, Dr. Don Cleveland and Holly Kordesiewicz. Sarah and Ed, Michael Hayden's group did some of the work. And CHTI was instrumental in funding, in particular Doug McDonald. And then the Hereditary Disease Foundation deserves a lot of recognition for getting us here and helping us along the way. Then my colleagues at Roshan and Ionis. Thank you. So I'd love it if people had questions for either Dr. Tillman or Dr. Bennett. So raise your hand if you have a question. Yes. Hi. Both of the presentations were fantastic. Thank you so much for explaining things so well to all of us. Dr. Bennett, I had two quick questions. One is when the strategy is to target just the mutant Huntington allele and not both alleles, why does the therapy only work on about 40% of the people? Right. So it has to do with, there's heterogeneity in these what's called single nucleotide polymorphisms, which are the single base change that occurs between all of us. And for a drug that targets a particular polymorphism, let's say it's a A, the other 60% of the population will have a G at that site and they won't be treatable. And so there is no single polymorphism that links 100% with the mutant Huntington allele. And so we're playing a genetics game that there was some diversity in our lineages that got us to where we are today and some of those we can exploit. But unfortunately for Huntington's it's not one that would be universal. We would only treat a subpopulation of the patients. Thank you for explaining that. Also, when are you expecting to start recruiting for this phase three and are the sites that will be participating already listed somewhere? No, the sites aren't listed. They're our partners Rosha are responsible for this so they're taking it on. They're interviewing sites as we speak to see which sites want to participate and then they go through a qualification for the sites to show that they have the staff and the infrastructure to be able to support the clinical trial. That's going on today. We expect to open up some sites in the U.S. by the end of the year and perhaps start dosing either, I suspect they'll start dosing patients at the beginning of next year, just given the holidays, but it's imminent. And there's a website called clinicaltrials.org that you can look on to and once there's a site that's. .gov, I'm sorry, clinicaltrials.gov. You can look on to and once the site is active they'll list there and then they'll also list the coordinator who to contact to, you know, if you wanted to participate in the study. Thank you. Any other questions? Yes. Hi, Dr. Bennett and Dr. Tillman. Thank you for a great presentations from both of you. My question is to Frank and Frank, if you had a crystal ball and I know you don't, but if everything went well with the ASO trial, when would you expect to see it approved? Yeah, so that is a crystal ball and again I just want to emphasize we're still very early. So there's lots of opportunity for things to go wrong because I don't want to overpromise, but the plan would be this trial would take probably three to three and a half years to finish and then once it finishes and you get the data, if the data is positive you would file with the regulatory agencies. I suspect given the need for therapies for Huntington's disease, the regulatory agencies will be very responsive and probably approve it within six months of filing. So generally it would take after we got the data, it would take three to four months to get all the data organized in a way that would allow filing and then another three to six months for approval if again assuming everything went well. So we're probably talking four years for a little over four years. Thank you and again thank you both for great talks. Could you comment, Frank, on what level of illness manifestations characterized the group that you preferably are going to work with this drug on? Right. And then maybe make a comment on if let's say hopefully things go well, how you then think about more serious people and perhaps people who don't even have the manifestations yet. Yeah, so this clinical trial is in early manifest HD patients that I need Dr. Young to explain to you what that means. But it's early stage patients will be in this trial and I don't know if you want to add some color to what. Oh, sure. Well, I mean, we have ways of assessing people both in terms of standardized tests of the motor system as well as standardized tests of the way we think and put together thoughts. And we know that there's a long period of time before you actually show the symptoms. Dr. Tillman showed that where things are changing in the brain, but you haven't got overt symptoms yet. I think what they want for this trial is to get people who've just fallen into those early symptoms where you can just start to see motor abnormalities and not later than that because then you wouldn't be able necessarily to revive dead neurons, but sick neurons. Yes. Yeah. And so the plan is to go both directions. Actually, you know, I think as Dr. Tillman pointed out, the future is really in prophylactic treatment. And so I really do see the presymptomatic treatment as a direction that we'll head. But first we have to demonstrate the drug has some benefit to patients. And then also I think we need to ask the question, what is the benefit in late stage patients? And so I see that happening. And then finally, there's a juvenile patient population that, again, I think we'll want to explore at some point. I have a question for Dr. Tillman. My daughter wanted me to ask this, so she's so shy. But you talked about there's other genes that affect the onset of Huntington's disease, which is the first time I've heard that. Could you just talk a little bit more, what are the genes affect the onset? There are, I think now four or five that have been, how many, Tom? There are five. How many? Fourteen. Fourteen. Fourteen. Which is, which is a lot, but it's going to give scientists tremendous opportunities for two things, I think. One is, what do they tell us about the biological function of the HTT protein? And that matters a lot to Frank, because we're here to develop strategies that actually reduce the level of both the normal size protein as well as the mutant protein. It's possible that that could be deleterious for a whole entirely different reason that you're losing the activity of the wild type protein. You know, there's so much that apparently is not known about what the normal biological function of HTT is. So I think these gene candidates are going to give us a lot of information about just the basic biology of what is going on. But then the really exciting thing, and I didn't emphasize this, so thank you for the question, which is that some of these, the variants actually prolong the period before disease onset. So those are the ones you're really interested in, right? You want the ones that are actually extending the time before symptoms occur. So if I were to prioritize those 14, that's where you would begin by prioritizing the ones that have the greatest impact on extension of normal function. No, I agree. It's very exciting, and it gives us not only us, but other companies as well, for the opportunity to have drugs that will impact the disease, and I think it's really critical. The one other thing that I would add, and this may be more than you wanted to know, but one thing to remember is that this protein is made in every cell in our body. Yeah, now it's pathological effect when it's a mutated form is in neurons, but we don't know much about what it's doing elsewhere in the body, and it would be good if we knew that actually. The second is that what we do know about the protein, it appears to be a protein that for better use of a word is kind of a scaffold protein. It interacts with a lot of other proteins. It may be a protein that moves them around in the body or in the cell inside the cell, but again, because we don't really know that, it's very hard to think about the impact of some of the kinds of therapies that could be considered. So these genes are, they're like clues, right? And it's wonderful to be able to have clues to function. I just might add that part of the structure of the workshop this weekend was to follow up on the exciting work that Nancy and David Hausman have been doing looking at modified genes in the Venezuela group. And they've come up with quite a few and we spent all of yesterday and this morning talking about ways we can extract those as drug targets. I want to just ask you to comment on something that evolves from what you said. And that is, so we're seeing modifiers that can alter the age of onset of huntings. What do we know about how many other brain diseases or other diseases may be subject to the same kind of benefit? Well, all of them are going to be. I mean, to the extent that certainly of all the neurodegenerative disorders, every one of them would fall into that category. Yes, in fact, for SMA, we've been doing a lot of work looking at modifiers for SMA. And we've identified, we didn't, but a group in Germany identified a couple modifier genes that when we target them with our anti-sensologos, we further augment the activity of nuisance. So it's clearly a therapeutic strategy that I think the industry and we're very interested in. And this is a question for you. So aren't there therapies that are either starting now to be tested in study participants to actually go in on some of the other chromosomes where they've found these SNPs or these small segments that actually do perhaps that increase the progression of the disease faster in certain people than others who have the mutant gene where they're actually trying to turn those off. I think I thought there were a couple that are actually involved in the cutting and they're screwing up the cutting of the genes. Exactly. So the issue here is yes, there are genes that delay the age of onset further than you would expect just based on the CAG repeat number. And also genes that shorten it and make it earlier age of onset than predicted. Now both of those are drug targets. Right. And we haven't started testing them in humans yet. But again, a bunch of people at this workshop this weekend have grants to look at these very issues in DNA repair enzymes that make it shorter onset, you know. So there's a lot of work and it's going to be very exciting. So I'm going to say look, everybody needs a drink. Yeah, we can talk to each other. This is great. Thank you.


Welcome back to Think Tech. This is Talking Tax with Tom Yamachika, the president of the Tax Foundation of Hawaii. Today, we're going to talk about Kurt Krufella's special mission with regard to film credits in Hawaii. Welcome to the show, Tom. Thank you, Jay. I'm glad to be here. I looked up Kurt Krufella, and while he is a very publicity-minded person, if you Google him, you get a lot of hits. He's always on the platform somehow, but this one seems to be a continuing controversy that he has created. Can you talk about it? Can you talk about how the film credit works and what's wrong as far as he's concerned? Let me just kind of start by saying Kurt Krufella ran and won as a Republican, okay? And he's one of... He used to be the only Republican in the Senate. Now there are two, him and Senator Awa, which, interestingly enough, means that because of the policy that there'd be bipartisanship on every committee in the legislature, he's on pretty much all of the committees, including, importantly for us here at Talking Tax, the Senate Ways and Means Committee. Isn't that Donovan Delacruz's committee? Yeah, yeah. Senator Delacruz chairs the committee, but Favella does have a seat on it. He apparently has been persuaded by the Teamsters that there are problems with the Hawaii Movie and TV Production Tax Credit. By way of background, we've had the Movie and TV Production Tax Credit in place for a long time since, I believe, 1988. You know, it was in some years more, some years less, but the basic idea is that when Movie and TV Productions come here, they're allowed a tax credit based on what they spend here well, not necessarily here, but it has to be subject to our local tax, either a general excise tax, use tax, or income tax. The Teamsters believe that's not enough, and they kind of made a show of it this past session. We talked earlier about what happened with the Film Credit Bill with the Senate Wains and Means Committee grabbing something relatively unrelated, shoving a bunch of these changes that the Teamsters wanted into the bill. And when the House didn't hear it, they took one of the House bills and they basically shoved all those provisions in that one, much to the consternation of the House Committee. What did it provide? Well, for one thing, the bill provided differential tax credit rates depending on whether you have local payroll or out-of-state payroll. Let me stop you there and say, gee, that sounds like a violation of the United States Constitution Commerce Clause. Yeah, it probably is. I mean, I thought so. The deputy attorney general thought so. But did that modify the Ways and Means Committee? I don't think so. But let's go back to Fevella's film feud. So it's now after the termination of the legislature. On May 31, there was a press conference held at the Capitol regarding that movie and TV production tax credit. And two of the main speakers were a gentleman from the Teamsters, a gentleman named Kevin Holu, and Senator Fevella. Now, Mr. Holu's basic point was that there weren't enough local Teamster members working in the productions. So they wanted, and it's no secret we've been just talking about this, they testified in favor of the predecessor to the bills that we were just talking about, urging them to amend the legislation by adding in safeguards to ensure that productions are engaging with local unions and hiring Hawaii residents and utilizing Hawaii-based businesses for goods and services. Safeguards, it sounds like a euphemism to me. Yeah, it actually is mandates. It's not safeguards, it's mandates. That's what they wanted to put in. That's what they did put in. And of course, at that press conference, Senator Fevella got up to speak. And he had his own views about how the states administering the credit. This is Hawaii, he said. People were standing in line to film here. But when you get one person making the decisions, that's the discouragement. That's the guys discouraging people to come here. So what did he mean by that? Who's the one person? And what are the decisions? Isn't it just simply in the law? His beef was with Donnie Dawson, the head of the Hawaii Film Office. She has been the head of the Hawaii Film Office for like 20, 25 years. Yeah, but to emphasize the point, he filed a formal personnel complaint against Ms. Dawson. And that's kind of working its way through the Department of Business and Economic Development right now. Saying what? Saying that Ms. Dawson misled legislators by describing what the bill would do. That's interesting. Yeah, I mean, during the time that when the bill was out, the MPAA, among others, had some complaints about the bill. We did, too. We had some concerns about constitutionality over the Commerce Clause, as you just mentioned. Basically, what the Commerce Clause says is that we in the US are supposed to be one big happy family. So you have one state and another state. We're all in this together. We're paddling the same canoe. We're all one ohana. So one state shouldn't be discriminating against commerce coming from another state. But that's exactly what the bill did. And it was very explicit about it. So is that what Donnie Dawson was charged with, testifying that it violated the Commerce Clause? No, I think she made some other points that were kind of consistent with what the MPAA was saying. I believe in civil beats coverage, they did have a copy of the handout that Ms. Dawson gave Senator Fevella and others. Just as an explainer to what the industry position was. Now, let me boil this down just as far as our conversation is concerned up to this point. This controversy is about requiring local union labor in violation of the Commerce Clause of the United States Constitution. And so one side of the controversy is, yeah, we should have local union labor in violation of the clause. And the other side is we shouldn't because it violates the clause and I suppose other industry considerations. Is that the controversy? Well, there's two parts to it. One of them is that part, right? And of course Senator Fevella's rejoinder is that working with mainland companies, managing studios and production at Huy, you don't want to have a problem. Everything should be local. It's our land, it's our police, it's our people. That's basically his argument. I saw him quoted for that in the civil beat article. That was extraordinary. That's what he's saying, but we do have the Commerce Clause and I don't know if Mr. Fevella recalls this, but when he was first sworn in as a Senator, he had to take an oath to support and defend both the Constitution of Hawaii and the Constitution of the United States. Well, the Constitution of Hawaii calls for a compliance with the Constitution of the United States. Doesn't really have to, but it does. And article 16, section four of the Hawaii Constitution calls for every lawmaker to take that oath. So is he alone on this or are there others who join him from the legislature? Well, I mean, obviously there were others in Ways and Means Committee who were kind of singing the teamsters tune, right? It takes more than one person to do those kind of legislative maneuvers, but you have to kind of look at the reality and the reality isn't that people are lining up on the door, I mean lining up to film here. Do you remember Jason Momoa, Hawaii-born actor? He made it one of his life projects to film a Hawaiian historical drama. Chief of war. Chief of war is what it's called and that series is indeed being shot now in New Zealand. Yeah, part of the film was shot in Hawaii on all of the major Hawaiian islands, but as it turns out, a good part of the movie is shot in New Zealand, a number of the principal cast members are New Zealanders, not Hawaiians. Why? It turns out that New Zealand offers international productions, a production grant of up to 25% on qualifying New Zealand production expenditures. That's better than a tax credit. Apparently it is because according to the producer of Chief of War, a gentleman named Brian Keaulana, he said, to survive, we had to go to Aotearoa, which is New Zealand, to survive for this. But by keeping the tax credit, it would give us the opportunity to keep us guys at home. Let's hypothetical. Suppose this bill passes, okay? And we have more local teamsters staffing these films to the extent there are films here in Hawaii. If they are, if the films come here. Well, I'm assuming that, okay?  They're gonna go to New Zealand, just like Chief of War did. There's many considerations, but let's assume, of course they do, they do come here. Let's assume, and this is a really big possibility, I mean, an encouraging possibility, there's enough talent right here in Hawaii to make films, okay, except they would have to use Teamster help, lots of it to make their film here in Hawaii. Is that competitive, or would that also force local filmmakers to go elsewhere? That's another dimension, and that definitely needs to be considered.  Yeah, that's what I'm thinking. The smaller productions are the ones I would care about most, but I don't think this bill would help local productions. This bill would impose a de facto obligation on every production to use Teamster help and to have more help. And the result is that nobody could make a film economically and to the extent to Hawaii might attract either local or out-of-state business, it would diminish. The other thing is, and I would like to spend a few minutes with you on this, it is troubling, is it not, to look from the outside in and see this obvious attempt by Pavella who is essentially working for the union, manipulate the law, so as to help the union and position the union to have more union members, more work, more local union members working on films that are made here. This is troubling in the sense that it doesn't look good from the outside. It looks like we have a problem in incentivizing moviemaking in Hawaii and the people who should be like Donnie Dawson who should be incentivizing, who should be managing the efforts of filmmakers to make films in Hawaii are not really in charge. And there's a statement here about our willingness to accommodate filmmakers of all kinds from Hawaii and elsewhere when you have the union running things and you have shouting and screaming and lots of newspaper articles about Pavella. And I'm thinking that if I'm a filmmaker in Los Angeles, I would say, gee, we've had problems in Hawaii before. We've had problems with tax credits in Hawaii. It's not completely predictable. We've had problems with the teamsters before. And I'm in LA, I would say, I'm not gonna do this. I'm gonna go to New Zealand right away. The weather is good in Hawaii, but gee, this environment is really not made for filmmaking. Yeah, no, I mean, there are, we're not an island unto ourselves. We have competition. We have Puerto Rico, we have New Zealand, we have other places in tropical climates. And of course there's the green screen, right? Any place, even in Los Angeles, can be made to look like Hawaii. And there's animation that looks like a green screen. The technology is extraordinary now. In the old days, the green screen would have visible issues to an audience, but now green screens are so effective you can't tell the difference. And beyond that, you can make the green screen better and better with animation. And again, you can't tell the difference. So there are so many options that are cheaper, that are open to filmmakers now. The technology really covers it all. Don't forget AI, Tom, because AI can generate scenes and backgrounds and all kinds of things that will help a filmmaker create an alternative set and scenery. So this is really foolish, not only to make an unconstitutional bill and push it and shout about it, but also to tell the world about our attitudinal problems. Yeah, I think it's very dangerous to make broad statements about insularism that, you know, hoys-hoys and nothing else matters. It's kind of like, make America agree it again, but on a smaller scale. Yeah, we have so many issues like this. You know, the whole affair, the OHA attempt to build a 40-story condominium on Kakaako Mackay, I saw that there are those who would stop the improvement of the Puna geothermal venture. And I'm sure that you recognize that the Manakea project with the 30-meter telescope, which would be a tremendous item for prestige for Hawaii, it has been stopped against all the findings, all the courts, all the arbitration. It ain't going anywhere right now and it probably is dead Mackay mort. And so, I mean, we have these issues where people want to advance, how shall I characterize this, local partisan issues in order to make it hard for people to do business, make projects, make progress. And it seems to be happening more and more. Think of the ferry. Think of the super ferries, another one. These projects all got stuck because of partisan issues like this one. Absolutely. And if we want to make Hawaii a business-friendly place, if we want to attract capital from outside, which is what these film projects do, okay? I think we have to be accommodating, at least to some degree. I don't think this is over, Tom. Of course it's not. This is just a symptom, not the disease. And it's really ultimately damaging to the film industry here, which is a great possibility for us. We should be inviting them from hither and yon. We should have films all over the lot. It makes so much money and it sells Hawaii, doesn't it? Yeah, and importantly, it brings in capital from outside of what we now have. I mean, we've always complained. I mean, we've heard lots of complaints over the years that Hawaii is capital short. Well, the answer is to get entities or businesses outside of Hawaii to invest in Hawaii and move your productions, one of them. And the other kinds of capital, capital would come in for the telescope, capital that come in for the super ferry. I could go on, all these are stopped and the capital doesn't come in and you start counting them up on your fingers and toes and it's billions and billions of dollars that had been locked up or rejected. You talk about Donnie Dawson and some of the filmmakers coming down and opposing this bill. And of course, the tax foundation opposed the bill, but is there an organization that would say, wait a minute, this is unhinged. It's not legal and it's not good for us. Is there an organization, kind of a chamber of commerce organization that would come down and oppose a bill like this and tell it like it is? Well, I mean, supposedly that's one function of the NPA produces or directors. It's more than tax and it's more than filmmaking. It's inviting offshore capital to come here. Yes, it should be managed. And I think Tech had a very interesting program about managing offshore capital 10 years ago and I thought that was really important to understand it from that point of view. We need somebody to A, advocate for bringing offshore capital here and B, managing it effectively. Well, I mean, supposedly that's what we look to our governor for. You know, when our governor there saying, this is the policy of the state, this is what we want to attract. You know, we love films and we totally support the industry's use of Hawaii to promote Hawaii. Come on down, we'll make life comfortable for you. We'll show you our local spirit. We'll show you our hospitality. Right, and what are the side benefits of all of that is that our budding filmmakers from the Academy for Creative Media, other places in the university, you know, all these filmmaking organizations that are small, they're low capital, small organizations in Hawaii, trying to make films would rub shoulders with, you know, more serious, more heavily capitalized producers from the mainland. And A, they could learn a lot. They could even just watch, but they could get jobs too. They could learn a lot and make a real industry here.  I think there should be a countervailing deal here in the next session that would further encourage them, not reject them, and at least we'll have two hands clapping, don't you think? Yeah, I mean, we have a film credit that's for better or for worse, survived more than 25 years. Why aren't we using it? We should be using it. We should be extending the sunset date.  Well, you know, it's a marketplace thing. If we find that producers going around us, going to Puerto Rico and New Zealand and what have you, and other places in Asia, I should add, Yeah, that's not their fault. No, it's the economics of it. That's right. So we have to get into the mix and be more competitive. That's simple. And it's a combination of things. It's not only increasing the film credit, but it's developing an attitude. You know, the aloha spirit, if you mentioned, where we demonstrate that we care about them and we support them and we help them. And we try to get jobs and internships and the like so that local people can learn from them. It's a very, as you said, it's a very highly technical business now. You know, you can't learn it by not getting close to it. You have to get close to it. Yeah, we ought to be concentrating on people like Chris Lee, who were in the industry and have come here to impart his vast knowledge to local people who want to get into the industry. We ought to be listening to him more. We need to kind of pick the industries that we want to help given that we've already picked this one. We really should be, you know, accommodating if we can. You know, we shouldn't be trying to kick them out. We shouldn't be taking the attitude that, oh, they're gonna come here anyway, because they won't. And we're finding this out more and more as we've seen with Jason Momoa's experience. They'll go elsewhere. They don't have to stay here. And we should realize that, and we should realize that we're in competition to attract and keep industries like that. Thank you, Tom. Important discussion. Thank you very much. I hope that people get the message on this. Thank you, aloha. Thank you so much for watching Think Tech Hawaii. If you like what we do, please click the like and subscribe button on YouTube. You can also follow us on Facebook, Instagram, and LinkedIn. Check out our website, thinktechawaii.com. Mahalo.


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Beeper says this new app has reversed engineered how iMessage works. Can do group chats, high res images, high res video, voice messages, stickers, gifts, reply threads. Beeper figured out how to craft an SMS message to register your phone with Apple Surgeon. The server then registers your phone number as iMessage capable. There's a lot of questions you may have like, is that secure? Well, it's tight. It's from your phone number. So it can only work with your phone number. You don't log in on that cloud server. You log in on the app on your phone with the Beeper login, not an Apple ID, and then you get a credential from Apple that says, oh, you're the you're the person I'm going to send these messages to. Here's the credential to get the notification. All it can do with that credential is ask the Apple server to send it a notification that a message has come in. It cannot use that credential to get your actual message. That credential to get your actual message stays on your phone.


On the breakfast Nigerian aviation increases transportation fares, making so many Nigerians furious. Rev. Gavna Yesomuike has accused his cross river counterpart, Benayadi, and the police of attempting to prevent the People's Democratic Party from holding its rally for the Egoja Yela Federal Constituency in Aqabaio State by constituency or by election in Calabar. And as always, we'll be looking through the national dailies this beautiful morning. Rev. Gavna Good morning to you. It's great to have you join us on the breakfast right here on Plus TV Africa on what's a beautiful Tuesday morning. My name is Kofi Bartel. Rev. Gavna And I am Mesa Bokwos. Good to be back on your screen. Rev. Gavna Yes indeed. And of course we're back. Thank you for a brand new day of conversations and analysis on the important national issues that our listeners, viewers, rather would like to hear about and also discuss as well. The issues are still the same. You know, talking about the petrol queues, it seems they're dissipating, though that's not something we're looking at today. But the price is still high and people are paying a bit higher. But apart from what you and I buy, which is petrol, those who buy diesel have been complaining. And now, those who are buying what we call jet A1, aviation fuel, are complaining and it seems that they are going to be through the burden back to the final consumer. We'll look at that as we go on. But it's a worrying day. Are we all going to start travelling by road again in these times? We'll talk about that as we go on this morning on the breakfast. Of course, I'm looking at what's happening in Cross River State. I see that it's here to you and I, isn't it? It's always small. Anyway, let's get into our top trending stories this morning. I am ready to fight dirty Bola Metinbo. I am ready to fight dirty Bola Metinbo. That's not just the only thing he's quoted as saying over the past 24 to 48 hours. He's also quoted as saying that the young people of Nigeria, the youth of Nigeria, should wait for him to be president before they become president. I think he may have meant it as a joke, but sort of we're selling himself to the young people. Not a few Nigerians have not found it funny. He spoke in Yoruba while paying a visit to the Alaafi of Oyo. His Royal Highness, the Alaafi of Oyo. And he told the young people gathered there that they should make a way, clear the road for the elders to pass. After they are gone, he's gone, they can now come in to be president. He said that jokingly, but some people have said that Bola Metinbo was a leader in his youth. In 1999, when he became governor of Liga State, that's how many years ago. That's almost 23 years ago. Yeah, that he was in his 50s or 40s, you understand. And even before that, he was a senator in the previous republic and he was young. So if he went out and he vied for such positions, why is he saying the young people should wait for him to become president before they become president? And you've had to discuss these things over and over again. But some of his supporters, those who are sympathetic to his view, say that well, he was only making a case for himself to say he would like to be president and that they should just basically selling himself. Also, that's not the only statement that he's quoted as making. Apart from visiting the Alaphio over here, he also paid a visit to the Olubadon, Designate. It has been back and forth and a bit of a tussle, but we're not having Olubadon. He will soon be being installed. And he is quoted as saying to the Olubadon, Designate, that he's ready to fight dirty. He's ready to fight dirty. And let's roll the tape. Okay, and this is no longer tape. Let's roll the tape and let's listen to the man himself as she was you. Bola Admitinobu. Oh, Admitinobu. It's not all about insults. Now that may, I'm ready to listen. And I was saying no more, I don't want to listen now. I've read somewhere in a Greek philosopher's book, who said if you want to raise up with pink, you're ready to get it. You're ready with the book. I'm ready to get it. All right, so it's quite interesting. A lot of people have picked an issue with that. Those words, I'm ready to get dirty. And they're looking at it negatively. Some are looking at it as well. He's just saying if those who are competing with him, maybe the pigs refer to them, not directly, but you know what I'm saying. It means people who are dirty in nature.  But majority of those who have been commenting think it's a negative statement. It's potents maybe underhand tactics or negative stuff during the elections or maybe even violence and all that. And some people are saying, oh, we saw M.C. Oluomo the other day saying that arranging his boys and strategizing. So he's going to be dead to you. Nigeria, you've got to get your PVC. And let's fight these dirty politicians and all that. So it's been a back and forth between those who are proteinable and those who are anti-snow. But I mean, it's trending. For instance, Renault Mokri has had a field day on Twitter talking about Tilebu playing dirty and all that, asking several questions about it. So it's not been too much of a good PR day for a few days for Bola Mettinbu. The young people now are trending answers. The young people now are linking his statements to answers and to what happened there. His name is family and the legal state government and political establishment as a whole being identified with the answers, you know, massacres if you want to call it that. So maybe his peer guys need to do a heavy page. So it's actually not very strange that that kind of politics that we get to practice you if you have heard the Machiavellian kind of theory. There you go again. No, no, but that's real. And the crux of everything is leadership stuff. Have you heard? Yes, I have. A little bit of it.  And so however you get it, it doesn't really matter as long as you get it. And so that's the kind of politics.  It's just what it is. I'm ready to get dirty. And what does that mean? Whatever it takes to get it, I will get it. And that's it. The goal at the end of the day is getting it and not how you get it. And that is actually not new for us in our politics. In Nigerian politics. Exactly. Because we see all of that. I mean, we see the thogry. We see how these politicians and those who are aspiring would go to any length just to acquire power. It doesn't really. So there's no morality in this conversation. And it's not a new thing. But we're hoping that we gradually get to that point where there's morality. Some people will say you cannot. You can't practice politics and morality at the same time. And so yes, this kind of theory has been imbibed by some of our political, you know, what you call them, elites. They go a long way. They can do anything, whether fetish, whether. And some of these things you would, a lot of people can actually, you know, relate with them. Some would go ahead as far as having thugs and what have you to truncate the system. So it's the interest. It's what they want. And that's what it is. So it's really not new. But we need to also understand the fact that until we, the people, understand that power resides with us, that the people have the power, until we begin to, you know, kill all of the sentiment. Yes, we understand that there's a trust deficit in the system. A lot of people no longer trust the system, the electoral process. But hey, and that's why people don't come out. So all of the elections, you want to look at it from, I mean, 1999 and all of these elections that we constantly have, one of the things that has always been constant is the fact that you have political apathy. People don't like to turn up. People's participation is really, really nothing to write on about. Even with all of the buzz on social media and all of that, at the end of the day, does that translate to people turning out and showing up to vote and exercise their rights and franchise. Now, they already understand, because it's a game of numbers, if the Nigerian people understand that they show up, it would be difficult for these persons to manipulate the system and try to override the figures and what have you and steal it. So until Nigerians understand that power is in their hand and decide. Now, on the other hand, the truth is everyone has a right. Like we talked about it. I think we've actually mentioned this when we had the 102-year-old woman who is actually a second female, was declared her interest to become president of Nigeria. Some people would have said, oh, it's in different strata, different meaning. Maybe she just wanted to prove her point and what have you. But the point is the Constitution gives everyone a right. You have a right to vote and revote it for. And so as long as you are of age and talking about age now, there's no age barrier. So like, okay, so you have that age as long as you're 18. Age limits, yes. Yes, age limits. But you don't have any restrictions saying when you get to a certain age you can't contest. So no one has said if you get to 100, you get to 170. But naturally, the reason why a lot of persons have actually spoken, because if you follow the internet, I mean, if you see the boards across different space and reactions from Nigeria, you'll find that a lot of people have been very particular about it. Not necessarily that age is a bad thing. I mean, as we grow, we're going to age. All of us are going to get very old as part of life. It's the process. But the argument over time is that as you grow old, your capacity to perform, you know, drops. Physically, your body degenerates. I mean, you ask the medical practitioners, all of the system begin to slow down. And so everything is going back, you know, the other way. And that also... How does that connect with that? No, because it's a performance thing. So some people would say, for instance, now, you have seen Bola Ahmad, I mean, two weeks in, two weeks out. And so that's what people say. So you have two weeks in on the campaign. And on the other hand, you have to run, you know, probably go have some medical checkup. You may not be too strong at this point. Because age is telling. And as much as you can't cheat it when age comes. So some people are saying that, hey, for a country as Niger, you need someone who can be... That's the system. I'm not a medical practitioner.  They degenerate. And that's what happens. Memory, you know, sometimes, you know, a lot of things you probably will have a little bit of loss of memory, not necessarily because you're running mad or anything is wrong with you, but it's part of it. You're already getting very old. And it's not a curse. It's a blessing. It's part of life. But we need to know when to take a bow and walk away. And so we will, for a country, 211 million people, we need someone, we need someone who, you know, would be there thinking everything. Yeah, that's it. But you see the problem that we have just before Eletchia Inn now is that we constantly have people who do not put the interest. Kofi, the day Nigerians will begin to have leaders who put the interest of the people above their interests, above their interests, then Nigeria will become a great nation. Now, all of the things that we constantly say is as a result of, you know, personal interest. Personal interest, for instance, you have 100%. Personal interest is 80. The national interest is 20. Where does that leave us? So you see the governors. You see the contractors. You see whoever is in charge of anything. So your being is just that your personal interest is more than national interest until we get to that point where we're very patriotic. We have leaders who think about the people and would constantly put their interests, I mean the interests of the people and the nation above their interests, not just their interests. Now in the kind of politics that we will preach, you have people not just representing their interests but the client. And so when you have the politics of God, fadarism, some people put you there, you would be representing their interests. You do what they say. It doesn't necessarily matter about the people. But however, it is what it is.  Maybe the response sometimes could be overblown. You know, I mean it's true that you don't want to hear politicians say, you know, I'm going to fight dirty. But it's part of the game, like you said. And then whether they say it or not, it'll be dirty, you know. It depends on the extent to me of the debt. That is debt? Yeah, for instance, I mean yesterday, the court, I think the Federal High Court also struck out via the citizenship case against Tikop Walker. I mean, since we're taking the court to prove that he was an Nigerian citizen, and the case was struck out. I'll be, it'll be hard to convince me that whoever took that case to court, you know, may have just done that because they just, you know, loved Nigeria and all that. Even if they did, I don't know if they were, they were, you know, encouraged by some politicians. All I'm saying is that even if politicians who oppose to a TIKO are not behind that case, it'll benefit them. So in a scenario where they have to support or to push something like that, they will. I'm not saying that's what happened. But I'm saying that people dig up stuff.  You know, it's safe that nobody can pick it up and dust it, because everybody has a file. You know, even in governance, we see that the government fights dirty. It's bad.  You know, you finish last. You have to do some hard things. You have to, it means you're decamping. If it means to, look at those politicians. And that's what we're saying. Look at those politicians who, when they, when they decamp, okay, or they lose out, they throw things at their party. Look at the APC in the state. The other guys have said they're going to show them shaggy. Look at the APC in the river state. Magnus Avey lost out. And he went to court and said, if I'm not going to get it, the party will not be on the ballot. But it was on the ballot. So it's part of it. But it depends on the extent of the dirt, you know, to me, the extent of how far you're willing to go. That is this. Yeah.  He said they should lock Hillary up. He called them her names, you know, brought up some allegations. Even before he became president, the same Twitter that Donald was, was lambasting. He used Twitter to rise to prominence. Remember when he was tweeting that Obama was not American? He was a foreigner. You know, some people consider that racist. And when he came into the House, I mean, the Republicans also fought dirty as well. They tried to, you know, impeach him.   Even videos where he said he was going to group certain parts of women and all that. It was played on CNN everywhere. It's part of the game. But, you know, it depends on what extent these politicians are willing to go in terms of the word dirty. If you remember, in Los Angeles, it was who said that the election was a do-or-die affair, you know. People read all sorts of things into it.   But, you know, that was not what he meant, you know. So, I do hope that when Bola Mettimbo says he's willing to fight dirty, it will be within the confines of the politics, you know, not something that would disenfranchise Nigerians of their rights or scuttle the nations. Not necessarily that. You know, so anyway, let's move on to the next one. Abba Kerry. Sue's federal government seeks for freedom from detention.  He's embattled, and he's been taken to court. Of course, he's been taken in rather by the National Drug Law enforcement agency and them. Not a few Nigerians are surprised to hear that the man who has been accused of being part of a drug ring, the National Drug Ring, is now suing the federal government, demanding 500 million narrowing damages from the National Drug Law enforcement agency over what he terms his unlawful arrest and detention. In an originating motion, on notice filed before the Federal High Court in the Buja, he's also seeking an order directing the NDLE to tender a written apology to him in two national dailies. Of course, the motion was initiated February 16 and filed on February 17 by his lawyer. He's seeking an restraining order, an order restraining the respondent. This is NDLE, its agents, servants, previews, police or anyone acting on their behalf from further harassing, detaining, intimidating, arresting or him unlawfully. So I do not know how this will go, because it doesn't mean that if the police evidence against him or the NDLE or EFCC, that they can't arrest him again, they can't detain him within the lawfully or legally allow them time frame to question him. They can't, I mean, they can be arrested again. But anyway, the word he has unlawfully, unlawfully, so what is unlawfully? That is what is within the realm of speculation.  So we have to allow the law to run its full course. It won't be fair of us to sit down here and conduct the media trial on Abba Kerry. But of course, people have already passed the verdict, but we here, we know better than to. So the surprise there was that this man had your audacity to sue the federal government in the NDLEA. So I think he understands the system, he understands the law and how it works. Because usually, I mean, when you have to keep a person, if you should be able to establish all of the facts and then if, what he's trying to say is, where the facts establish it, and if there's a case, let's get to court. And that's what it is, I think. But however, let's see how all of this actually unfolds, like we rightly mentioned not here for the media trial. It has been innocent until being proven guilty by a court of competence jurisdiction. So and that's so, you know, it's almost very difficult to... He's within his rights. That's what I'm saying. Some people don't understand that, you know, everybody has, needs to have their same court.  The judge was interested in hearing them. Some people didn't understand why, you know, we're accusing his lawyer of wasting the court's time wasting taxpayers' money in talking about Namdi Kano's clothes, Namdi Kano's eyeglasses, Namdi Kano's, you know, sleeping issues. But nothing has changed. But the thing is, when you get to court, the judge will ask you, are you treated well? Is everything fine? And if you have any complaints, no matter how accused or guilty people think you are, you have a right to seek justice. That's why it's called justice.  That's why they are taking to court. Otherwise it would be jungle justice, which is just catching and throwing in jail, you understand. But that is not being done. So whatever Kari does is within his rights, I mean, the things that you and I will go to court for, you know, for instance, citing the international conventions on human rights and all that, that people like you and I, Abdi Kari is within his rights to apply for this. And I think let's allow the court to its work. Definitely. Well, that's the size over conversation on top trending. Tomorrow we'll return with more interesting conversations, making the rounds in different spaces of the country. We will definitely step on the break. When we return, it will be time for us to be looking at the top stories on our national daily, as we call it, the newspaper review or off the press. We stay with us.