Okay, good morning. Thank you to the organizers for inviting me, and as I was telling a few people, it's been a long time since I've attended a pure genomics meeting, and I sort of forgotten meeting I go to more human genetics and genetics oriented meetings, and I've forgotten how much fun this used to be, or still is, I should say. So, given my current perspective, what I thought I was going to do is speak to you about a specific example that I think will exemplify many of the problems we already discussed yesterday. So I'm not going to speak specifically about ENCODE, but rather how ENCODE kind of data are leading to the solutions of problems that we simply didn't have in human genetics. So to give you a perspective on disease, at least what the disease community, or people who are interested in the pathophysiology of human disease, what is it that they want, and why it intersects so strongly with genetics, is I've sort of used a quotation from, really, in medicine, a very well-known book by Barton Chowz, who used to be a colleague of mine and has passed away, unfortunately, a few years ago, and I'll recommend this book for you, it's called Genetic Medicine, a Logic of Disease, as to that's what genetics can provide. And he poses three very simple but cogent questions that patients want to know, and of course we as scientists wish to answer, which is why me. Why this disease and why now? And if you think about it, you would appreciate that the first one has to do with a question of genotype, the second one has to do with specificity, and the third with many aspects, but clearly epigenetics and environmental factors come into play. So I think for a long period of time we've been preoccupied, really, with just mapping human disease genes, both simple and complex, for a very simple reason. This was a very, very slow task, and you can't do genetics without at least knowing what the unique identifiers are. And ENCODE has now pushed us into this much larger land of trying to understand how cis regulatory elements or enhancers, as just a shorthand, can provide us a view of disease that we never really had. And I think we all know that even though we are in the very beginning stages of just doing a simple intersection of finding sequence variants in various kinds of motives and cis elements of some defined function, that this is really very incomplete. What we would want to know is answer the question of much more mechanistic and qualitative term. And these issues have already come up in the meeting yesterday. So I'm going to give you some reasonable speculations on complex disease genetics, say, after 10 years or more, a long history of Mendelian genetics, and 10 years or more of many, many groups around the world trying to do GWAS kind of mapping and probing the answers. And the first one is that it's quite clear that there are many, many genes, as originally expected, anywhere from hundreds to thousand, height already has 800 sort of identified SNPs or more in different locations. So each trait is going to be composed of many, many different components. Even though we sometimes focus on the statistical aspect of how much of the phenotypic variants we've explained, there's a whole variety of analysis very well done that actually sort of emphasize the fact that common variants, those say with the frequency about 5%, 10%, that in many cases they explain at least half of the trait and disease variation. We haven't found most of them. And this is where encode, of course, in reverse can be very, very important. And so the question is, if we don't have the statistical power to map them individually, which is the third point, we might never be able to find all the individual SNPs that contribute individually to height or diabetes or hypertension, let alone even the rare ones, so we have to find other ways of doing it. I think at least much of our data has suggested, and clearly most of the mapping data that each locust that's been mapped by GWAS, they may in fact have more than one culprit gene in many cases. And clearly there are many, many individual SNPs that contribute to the observed association. And so one of the really big challenges is how do we get to the true genetic structure for each given gene and locust that we come across. And at the end, I'm going to come back to this issue that we've done genetics. We understand the importance of the recombination map to focus on the bit of the genome where a particular part or a phenotype maps. But I would ask you to think, and I think we should argue for a while, that what ENCODE has brought to us is the idea of physical interactions between distal elements and a gene. And so we have to consider the physical distance. We will have to step out of the genetic recombination haplotype, a haplotype, as I will show you in my example is often really defined by the functional piece of DNA that is relevant, not only what the recombination distances are, that we've statistically focused on. So here's the example. We've studied this phenotype for many, many years as a model to understand what really happens in complex disease genetics. And many of the things that, or I should say aspects of complex traits that we take as given today, we've been able to show using Hush-Prince disease as a model for actually many years. I'm not going to talk much about the phenotype, except to say that what it is is a defect of the enteric nervous system. Most of us don't think about the fact that we have an intact, almost independent nervous system in our gut, and this is a disorder in which these children are born with absence of the enteric nervous system in the gut, which leads to a functional obstruction and needs to be repaired and there are all kinds of other consequent, both problems that comes with efficient repair as well as without repair. As disorders go, it is relatively rare. It's about one in 5,000 live births, but this of course is 10 times or more common than most Mendelian disorders. It is clearly multifactorial from a variety of evidence. It's got a 4% recurrence risk and many, many other features that has allowed us to probe the genetics. At a molecular level, the study is done for a long time. We know three essential bits, and the three essential bits is much of the genetic defects that we've known arise because of defects in two major signaling pathways. Is this the one? The one in the middle is the laser end. We occur through two major signaling pathways. This is a receptor tyrosine kinase pathway mediated through RET, and this is through a G-protein couple receptor, the endothelium type B receptor, and all of the other components, and I'm not going to go into details. There's very strong epistasis between these two pathways, and we have a crude understanding as to how this epistasis arises. The second feature that is quite strong is that the disorder really occurs because of an interaction, or I should say failure of an interaction, between what these cells of the gut meson kind do. They actually secrete many trophic factors. Now we know they secrete other factors that are important for the maturation of enteric neurons and the enteric neurons of the neuroblast themselves. We at least have a crude understanding of what the mechanism is. That is, if you have a defect here or you have a defect here, that will lead to a failure of these two kinds of cells to communicate early in development. You get failure of these cells to develop and differentiate and proliferate and then differentiate, and you get lack of these cells, which is the aeganglionosis that you see in the gut. Third, there are many genes that we have very definitively mapped to, or we find mutations in Hirschsprung's disease, but they don't fit in this pathway. Of course, there are many, many other portions of the gut physiology that impacts on this that we're trying to find out, but basically, RET is the major gene, and I'm just going to tell you, and maybe in question and answer we can discuss it, that we now know that almost every Hirschsprung patient has a RET mutations. Most of them are non-coding mutations, but almost every one of them have. The essential feature for today's discussion is that even though it was found through severe syndromic forms of this disorder, we now know that there are many, many mis-sense mutations, they individually rare, none of them are full penetrance, and of course, we found analogous mutations in many other genes of the same pathway, SOC-10, which is its transcription factor, GDNF, its ligand, and GFRA1, a very important core receptor, RET, is sort of an unusual RTK in that it requires its core receptor. The surprise came in trying to explain Hirschsprung's disease several years ago. There's a study that we did originally with Eric Green in the old days, when you had to clone out pieces of DNA, you had a sequence you had to do. We did multi-species comparative genomics to identify regions, which we then tested as enhancers, and we found a very common variant. It's about 25% in the general European population or those of European ancestry, but it is a gut-specific enhancer. It is bound by SOC-10, and this polymorphism disrupts this binding and leads to low penetrance, but still quite highly important mutation or variant for this disorder. Interestingly, it shows this form, that is, a coding is involved in the long and severe forms, whereas a non-coding is involved in the short segment of the much more common forms. Because of this finding, we argued recently that because we knew of other enhancers in this region, that any regulatory variant that would reduce red expression, which this one does, which clearly all these other coding mutations do, should have similar effects. So the idea is if we can find one loss of function mutation, any other loss of function mutation that would lead to loss of red expression, even through non-coding, should lead to that. And this is where this stands from the screening, and you can imagine that ENCODE has played a, this is just a summary, has played a very big role in this. We now have three such different non-coding polymorphisms. Here are the RS numbers, which I never remember. Red plus three is the one that sits in the first large intron of red. These two are further away, as you can, I think there's a distance here. This is, so this is roughly 10 kb from the transcription start site. Red minus one is a non-coding polymorphism that's much further away. It's about 125 kilobases upstream. This is about 18 kilobases upstream, so closer to red. They have very large allele frequencies, and here are the odds ratios. And these odds ratios, by any count, four or close to two, are really phenomenal so far as complex disorders go, which is why it makes this as a model. But if you did a genome-wide association study as we did, this would clearly be recovered. In fact, we found this quite, which is why we found it early. This one was recovered from a genome-wide association study. You would not take this, because you would say, well, this is just another polymorphism that's in high LD in some sort, and of course it is not genome-wide significant. And the point that I'd like to make is once you get close to a locus, you have to try and interrogate the effect of many other polymorphisms that actually do interrupt the known elements. So here is what we did in order to find these three, that is throughout the region, we did a much more forward kind of screen by looking at, we looked at 125 SNPs that were all of major frequency that were peppered through this region in encode-defined elements of various sort. 34 of them were Hirsch-Prung's disease associated, that is by conventional GWASP value. Eight of them lay within chip-seq peaks. In the specific cell line, there's a human neuroblaster in the cell line and sort of relevant, really a relevant cell type in that sense. And all of these were enhancers, these GRIS enhancers enhancers, we really identified the hard way in this collaboration with Eric Green about 10 years ago. And what we find is three of them also showed allelic differences by doing various kinds of reporter assays. I think the effect sizes here are all substantial, not only individually, but combinatorially. So these, they are in a region in which there is some residual linkage to sacrolibrum, but as I will show you that the effects are not all at the same time in development, they act in different times in development, in different combinations, and that's the basis for finding genetic interactions even between these non-coding elements. You know, these SNPs show significant levels of LD in the sense the R-square is small, but they all lie in a pattern and therefore they're relative to sacrolibrum, they're all large. And therefore what we can do is to identify a major source of misinheritability of this locus. So I'll very quickly go through. I think I've generally explained this. So here are the three polymorphisms. In this particular case, many of these DHS sites and other sort of histone marks that came from the, both encode as well as some from the roadmap project and this is an intersection of all the SNPs that I told you about that anyway led to those three. If you looked at the transcription factors as well as if you looked at the sequence that was right under any of those SNPs we found, we'd known before that red plus three interrupted a SOX-10 binding site and this one suggested that it was a retinoic acid receptor site, later that we proved was RAR beta and this one was a gata site. This later shown to be either gata two or three. In fact, we find effects on both. So these are just Luciferase assays to show that these three elements, at least apparent control or wild type form, they do show an effect, an enhancer effect. So here's the, I will keep calling is that a genetic sort of wild type versus mutant forms or the control versus variant forms. And as you can see, it actually scales fairly well with the odds ratios and we have now done many more of these studies. By the way, some of the studies involved only two of the SNPs, some three because we're in the middle of completing all of this. But even when we take all three, we have synthetic constructs in which we can assess reporter activity of combinations of these SNPs. And here is the haplotype specific odds ratios that we can measure in a population of about 600 to 700 patients. And what you find is a log ratio or a log relationship as one would expect if you assume some aspect of mass action. So the first two elements that we discovered not only showed reporter activity in vitro that was done in a mouse neurobestrom or cell line called neuro2A, the new one is much, the human line is much better. And what you can see, hopefully you can see that the enhancers in fact, are found both at 11 and a half and 12 and a half. But red plus three, which is the Soxton bound enhancer, by the way, it's found in not only the gut but in other cell types that's of importance in the development and where red is expressed that is in portions of the forebrain and in fact in the dorsal root ganglia. And what you find is the first enhancer is active both at 11 and a half and 12 and a half. The distal minus one enhancer is found at 11 and a half and not at 12 and a half. In fact, if you do measure gene expression of the cognate transcription factor, RAR beta is expressed at 11 and a half and not at 12 and a half. So these obviously do act as enhancers in vivo as well. And this is to show that the effects are specific. That is, I told you the Soxton form and the RAR beta and the Gata 2-3 transcription factors. This is doing knockdowns in doing SIRNA knockdowns and this is all done in neuro 2A. And what we found is the expected result that the positive control or the negative controls in this case work. If you knockdown RAR beta obviously gene expression of RAR beta goes down as it does in all of these cases but what's interesting is when you knockdown Soxton red goes down as it should because it's the transcription factor but when you knockdown red what you find is Soxton goes down. This suggests not only the same is true for Gata 2 and 3 so this suggests that not only are these the transcription factors that regulate red but red at least has a feedback effect at least on the Gata 2s and the Soxton transcription factors. These are just not artifacts of any particular cell line. We can show these results by looking at a retinol and a ret wall type mouse embryo from the same early time in development and I'm not gonna go through the details. This is just to show that this effect that we found in cells can be recapitulated in vivo as well. So I wanna make a final point that one of the kinds of tests that we do in order to show specificity is that the transcription factor effect when in fact you do knockdown is specific for the so-called wall type or the native form of the enhancer. And this again shows in a number of cases. Let me see, I think my eyesight is failing me that I'll take the big one here that even though I think this is the control that when you do the Soxton that what you find is a difference that you find it on Soxton and I'm sorry on red but you don't find it on these ones because you find that the difference that you see on knockdown is equalized for the wall type form. So in this particular case, what you find is that quite interestingly and other data that I haven't shown you is that all of the variants that lead to Hirsch-Prings disease in this case that the effect all components of red signaling. This is sort of written in the form of these are the three transcription factors. Obviously they make the cognitive proteins and they regulate red. This is the part of red production that is important and I gave you some evidence that red in fact signals back and in some ways controls at least these two transcription factors. We also know that if you knockdown red or if you look at the red Null mouse embryos that they are negative regulators of its own ligand as well as its co-receptors. So this fact is, so this is another level of control on red. Finally red is only active in its dimerized phosphorylated form and this of course you don't want during early times of development you want tight control of this to control proliferation within the gut and so this form of red is rapidly in fact cleared. The signal is terminated through the action of an E3 ligase called SIBL and what we find is this is also positively regulated by red. So red is a particular case in which its production, its activation and its signal termination are all controlled through various kinds of enhancers and one of the interesting things is that we find that genetic variation in all of these components through its non-coding elements is an important part of this disease. And the total effect therefore depends on the total degree of loss of function. So I'm just gonna end with a couple of sort of pleas really that in order for us to understand even this relatively simple disorder I think it required us to understand the rest of the network that is just finding a non-coding variant outside of red was not sufficient for us to explain the kinds of odds ratios, the kinds of patterns of risk that we see that are specific to not only haplotypes but also in the groups of patients that we have. So I think it goes without saying that since no gene acts alone understanding the functional context of its expression is actually very crucial for us to get eventually quantitative answers and that's what I mean by modeling and predicting what the consequences are going to be. And for this there's a lot of extensive literature that suggests that the gene regulatory network is in fact a fundamental unit to consider because of many, many reasons indicated here is modular parts of this network is in this particular case very highly conserved and there are of course a number of classical studies that have compiled much of this information. At least Eric Davidson argues that this comes in a defined number of sub-circuit classes so it's possible that we might be able to classify them in some ways. They do provide some system levels explanation of the development and physiological functions and I think there are many opportunities for mathematical modeling that can provide then the quantitative answers. And I think this finally gives us a way for understanding complex inheritance in a way that we haven't, we are still doing it on a gene by gene basis. Many of you in this audience would know the work of Iran Segal when he originally tried to model and explain gene expression along the anterior posterior axis during fly development. But this is a model, it's a thermodynamic model, it's fairly straightforward and I think this gives us ways not only in this case to look at gene expression but there are various ways in which what we are learning from ENCODE can be used to build mechanistic models for gene activity, for trade values in some sense. You'll hear Nancy Cox speak about it and eventually for categorical diseases, what matters, which is penetrance. So I'm just gonna end with a series of acknowledgments of many people that have helped us in these studies and I know that I was asked to answer some questions which I'll just keep out while I and sort of point them out as we discuss. All right, thanks. Just for the audience. Frequency and those kind of odd ratios. Oh, I got frequency in those odd ratios that for me suggests that this is under balancing selection or positive or something. Something must be pushing that allele, those alleles that are high or keeping them high. Is that the, have you looked at that? Is there an argument for that? Yes, so the original one which has the biggest odds ratio, clearly that SNP has republished on this before is almost all of the features of balancing selection. One thing that I should tell you though is Hirschspringer's disease was an effective lethal about right now 70 years ago. So it's gone from seeing only new cases or cases that were perhaps very, very mild and that had expression to now people living and obviously reproducing and passing the phenotype along. So whatever selection we are seeing obviously had to be, I mean, so in order to explain it, it's not a recent phenomenon. There has to be a long-term phenomena. And in fact, the allele frequency shows all of the features with surrounding at least some of the surrounding, you know, within the recombination haplotype. So no, we've speculated on this. I mean, the gut is a very favorite place for doing various kinds of selection. The second is we know of receptors that are null or nearly null that have like the chemokine receptor and the CCR5 that can act as, or prevent the entry of various kinds of pathogen. RET was considered to be only neuronal, but now we know that is expressed in other cell types, including the epithelial. So it could be, it has nothing to do with Hirschspringer's disease per se, but selected simply because of things like that. So, Mike will be real short. Everyone, we've lost the desk mic volume, so please speak up when you're projecting. Oh, ENCODE clearly helped us. What fraction of that? So ENCODE clearly helped us in the last two, the first one has been known for a very long time. And, but ENCODE also suggested many others. I think what we were finally helped by was the fact that originally we had a set of, I forget 10, like a dozen pieces of DNA that previously we'd also shown were enhancers. So I think the combination of that just gave us much more confidence of which ones to follow on. Thanks.


On this Memorial Day, we are called to remember. Call to remember the values we hold and the virtues we seek have been purchased. Call to remember the pride that we possess and the possessions that we collect have come with a cost. Call to remember that every challenge that we face and every choice that we make was preceded by someone who forfeited there. Call to remember that the freedom of every race and people in our nation today indelibly sits on the shoulders of every race and people who chose to pay the ultimate price yesterday. Don Nielsen has pinned a poem entitled, To Them We Ode. He writes, Happened today and in the past, Sacrifice made for hours to last. Wives to widows, Families torn, Gave their lives for them we mourn. Gone forever, Souls are lost. Freedom comes with this cost. Enjoy the life they did preserve. Fate they suffered did not deserve. On this day, lest we forget, To them we owe our life in debt.


a presentation of TFNN. The Tom O'Brien Show is produced every business day. Tom takes your phone calls toll-free at 1-877-927-6648 internationally at<PHONE_NUMBER>. Let's go to Alan Homosassa. Hey, Al, what's going on? Isn't it wonderful? This gentleman here with the golden report right before the market fell apart ended up with T-A-A-S. We have a 98% gain in the year. And I mean, we want 99% proof like Irish whiskey, but we had a good gain there. You always told us to do what we feel comfortable with. And if I lose a little bit of money on the table, I will. But I know that I just pocketed $8,000 or $9,000 in two weeks. That's a beautiful thing, man. Now, Tom O'Brien. Welcome, folks. This is Tom O'Brien of TFNN. We have five days a week. We go seven hours a day. We go 24 hours a day on the internet at TFNN.com. Always remember, folks, whatever you think about, you bring about whatever you focus on grows. Hope everyone's having a great day, safe day. It's making a great night and a great week, folks. Love is responsible for its actions.  And you are going to be going to experience the consequences of your actions in one way or another. All human beings are completely responsible for their actions, even if they don't want to be. Not good-wise, let's take a look at it out here. We have the Dow Industries trading up 11 Nasdaq up there. 14 S&Ps up one gold. Gold contract down $12.40. Traded $19.86 an ounce. We have silver down 13 cents. $23.15 an ounce. Light Sweet Crew up 58 cents. $81.90 a barrel. Notes and bonds. 10-year note, down 23 ticks. Trade in 107.20. 30-year of full point plus four ticks at 112.17 in Kingdala. Kingdala's up 204 ticks. Trade in 105.225. Euro at 107. Yen at 149. British Pound at 123 to 1 US dollar. Our phone number's<PHONE_NUMBER>. Give us a call, folks. One note's going on in your world. In the world of the S&Ps, let's take a look at it. What do you have? Last week, folks, market bottom-on, goes top-side, takes a huge amount of energy. And what you can see out here today, bottom-on is that when the spy goes from a price point of, in this particular case, what we went from $409 up to $435 in six days. So you can expect that you're going to be building cars. That's what we're doing. We're going to sideways move $0.45. You have 31 cents, but this is really an inside day. So it's 47 million shares. And I expect we're going to be building cars for a bit in order to basically get into the higher levels up here. That's most times when you get an acceleration like this. The bottom line is you get to build cars. Building cars is going sideways, pulling back with light volume, getting ready for the next leg up. We go into the queues. We take a look at the queues, same type of setup inside the queues. They're both higher but slightly. They're really sideways moves. The queues, up 71 cents. The queues did go over as high today. But bottom line, still sideways move. 30 million shares traded. Now the queues are, no doubt, much stronger than the spies. So the queues are at a much higher level. We go into the notes and bonds. And this is the number, man. Notes and bonds are the number. So what you're looking at here, you get the 10-year right now. We are yielding 4.65. And 4 points, well, it was actually 5.02, which was the high. Out here today, you're pulling back. You're pulling back with light volume. So we're pulling back 23 ticks. You got 1.4 million contracts traded. And if we take a look at this, this thing can get right down again to the 106.18.   You pull back to where basically it builds out of bottom. Now what's intriguing about the 10-year also, folks, is that the 10-year had the highest shot position since 2006 last week. And they had piled, the funds had piled into this like beyond belief. And that's exactly what you need for large turns in the marketplace. The bottom line is it blows my mind that they actually piled in at lows. But I've found that, yeah, professionals, I don't get it, man. They have a stock that's trading 100. All of a sudden, it gets down to 30, and they're piling in on the short side.  But that stat, that's 2006 to today. So there's going to be a lot of shot covering number one. There probably has been a lot of shot covering, but there's going to be a lot more shot covering. Notes and bonds won a higher price. We go into the gold contract. We take a look at gold. Would you have a gold? This is a big bottom line because sideways move again. You're down 12 bucks. But you can see that you're 1.3 million contracts out here. We're in the same area. Now, the cool thing about gold is this. Gold is Friday, you're pushing this higher swing, and you're pushing it with volume. So when you're pushing the higher swing either up or down, well, up would be a higher swing, down would be a lower swing. And you stop pushing with volume, your probability is going to blow right by it. So we'll see how this shakes up. Right now, you've got 1.3 million contracts that's going into basically 2.6 million contracts. So we're still consolidating out here, trying to get up and over this 2018. My take is that we're going to go to 2129 on the move that we're talking about right now. We get into King Dollar. King Dollar's the number man. You get the interest rate structure. So when interest rates go down, our bottom line will make currencies in whatever country you're dealing with weaker. So we have with King Dollar is, you're up 220 today, which is no big deal. But you've rejected lower price at 104, 684. My take is that we're going to get down first to this 104, 699. And what that is, that's where we broke out from. Took us a couple weeks of trading up, down, all around. So today, you did reject this 104, 899. So most times when you see that, you can see we broke that consolidation with conviction on Friday. So that is say the dollar can pop up to like the 106, 599. And that was the bottom of the consolidation. So you can pop up there, probably set up another ABC structure on the way down. We'll see how the whole thing shakes out. But silver, we're going to take a look at the silver market out here. Silver also, you know, last Friday we got a nice sign of strength inside the silver market. And today you're pulling back with light volume. So we take a look at this silver right now, you're back 14 cents. And you're going to see, you know, Friday we go higher with 100, no, 78,000 contracts. And today you're backing down with 49. That's a nice setup. That's a setup that wants higher price. We look at some of the higher volume equities out here today. And we have, you get Teslas down a buck. Nothing's really moving. Well, Apple's, well, let's talk about Apple for a second because this is amazing.  And, you know, as I said last week, if any other equity had full losing quarters, meaning in growth, which Apple did, this stock would get killed. Not Apple though. Bottom line is that it's taking out a swing point today. It has light of volume on the swing point, but guess what? Apple's Apple and people are looking full with an Apple seeing how many I-15s that Apple can sell. Stay right there folks, come right back. Tires, every Tuesday and Thursday, Tim Ord joins the Tom O'Brien show to share his unique insight that he's developed over decades of trading. Now on Tuesday, November 7th, from 4 p.m. to 5.30 p.m. Eastern time, Tim Ord will be hosting his own live webinar. Tim's analysis has been outperforming market returns by almost double, and his gold analysis is on track to be a winner as well. Tim will be delving into six secret ratios that every trader should know. In this webinar, Tim will be covering the daily TLT VIX, the daily and weekly SPI VIX, the American Association of Individual Investors bull bear ratios, and the trend panic levels. Tim will break down each ratio, how it is calculated, its importance, and how it can help you make bigger returns. It's as simple as this. Learn the ratios, trade by them, and see your returns. That's it. Visit the front page of TFNN.com today to sign up now. TFNN, Educating Investors. Currencies, commodities, and bond markets are as important as ever right now with how they're driving the volatility in equity markets across the globe, which is why it's a great time to try out Teddy Kegstad's Tiger Forex Report. Teddy Kegstad breaks down the forex markets every Monday using his 30-plus years of experience as a trading veteran of futures, forex, stocks, and options. Teddy releases his weekly Tiger Forex Report every Monday morning with coverage of all the major currency pairs, including the Dollar Index, the Euro Dollar, Pound Dollar, Dollar Swiss, Dollar Yen, as well as many more, and he also has weekly coverage of the crude oil market and the 30-year T-bonds as they both influence forex markets tremendously. When you sign up for the Tiger Forex Report, you also gain instant access to Teddy's 60-minute webinar archive. He just hosted forex strategies and fundamentals. What is behind the Tiger Forex Report? For all the details and to start your 30-day Tiger Forex Report subscription today, visit the front page of TFNN.com. TFNN, Educating Investors. Are you ready to take your trading to the next level? Introducing Tom O'Brien's award-winning newsletter, Market Insights, your key to successful active trading. Tom O'Brien, renowned for his expertise in the financial markets, has designed Market Insights to be your daily guide to profitable trades. 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Let's get over to our mammonster, Steve Rose, as we do each and every Monday at 20 past the hour. And don't forget, folks, Steve has an outstanding show here every trading day. 11 to 12, Eastern Standard Time. Also has a great newsletter, Mastering Probability. Now, it's very easy to get Steve's newsletter, folks. Come over to our website at TFNN.  You'll see it right on the right-hand side. You can get Steve's newsletter for one month for $119. You can get it for six months for $595, which is a savings of $133, and you get it for a year. No, sorry about this, man. I knew those prices were wrong. One second, man. Sorry about this, Steve. The heck did I just do here? Look at it so far. Where did I go? How did I just do this? Sorry, newsletters. How did I just do it? There it is. Oh, there it is, yeah. Can't believe I'm doing this. What is happening? There we go, nope. Okay, there we go. Sorry about that, folks, okay. Get it for one month for $149. You get it for six months. For $695, which is a savings of $199, 22%, and for one year for $1195, which is a savings of $593, 33%. Now what happens, folks, is that they all come with a 38-money-back guarantee. Steve has a huge amount of tools that he uses every day that you're gonna get as soon as you get the newsletter. So come on over, you get it for months, six months a year. If it works while you're great, if it doesn't work for you for some reason, just 28 days, just cancel it, then you charge nothing. Steve Rhodes, what's going on? Well, I think I have found a diamond in the rough in your neck of the woods in St. Pete. Oh, I like it. A real diamond. So I went to a number of concerts here over the last week. One of them was Saturday night, a group called Acoustic Alchemy, great jazz band. Most people have heard some of their songs, whether they know about the band or not. Okay. And I've seen them probably, they travel through South Florida once a year. So probably for the last five, six years, I've gone to see their concerts. And one of the founding members, his name is Greg Carmichael, great, amazing guitar player. But his wife is dealing with some major sickness and illness, and so he's no longer traveling with the group, so it's a little bit bummed about that. Well, turns out the guitar player that was replacing him is a guy named Nate Najjar. And he lives in St. Pete. He doesn't just live in St. Pete, he also plays in St. Pete. And I'm telling you, Tom, if you like guitar players, this guy is just extraordinary. Nate Najjar, I wanna write this down. Yeah, I'm gonna show you here, because I know we've got a number of listeners in the Tamp area. Turns out that he's playing, I guess in Clearwater, November 17th through the 19th, there is a Suncoast Jazz Festival. Oh, yeah. I think it was down, I think it was down just past the old office area. Yeah, it is, we can see it from the office. Yeah, no, no, I'm not sure, yeah, yeah, right. So there's a festival there, and he's playing at different times, so you can look that up. But he's also doing a Christmas, I believe it's a Christmas event on Thursday, December 7th and December 8th in St. Pete. Or it's, I'm sorry, December 7th is in St. Pete. So you can look that up, Nate Najjar, N-A-J-A. I mean, it is, he was amazing. So all of a sudden, that wasn't, so I always say everything in life happens for us. And really that was, so I was a little bit bummed that Greg Carmichael was gonna be there, but really what I got was a new guy to listen to. How cool was that? Yeah, and then last night, I went to see Special Effects, which is a jazz band that I've been listening to for 30 years, and I've never been able to see him travel. And one of the main players, his name is Kaylee Minucci. He brings out a woman to play the violin. Her name was Karen Briggs, B-R-I-G-G-S. Everybody looks it up, and she was amazing. My wife and I, we looked at each other, we're like, wow, never heard sound like that coming out of a violin in this jazz band. So, but finding this Nate Najjar. And most of these are small venues, Steve, right? Which is really cool. Oh, very smart. Right, yeah. Last night, yeah. 200 people max. Which is huge, which is dynamite, I know. Yeah, yeah, which is, it is so wonderful to see that. So I thought I'd pass that on to you. I couldn't wait really to tell you because I'm like, and then when I found out he was playing there, I'm like, oh, this is a beautiful thing. It's one thing to be a resident, it's another thing to play in your local community. No, totally, man, totally. All right, so that's beautiful. So last week, let's just get to the markets here. Last week, the spies, the cues, the diamonds, and the IWM form weekly, Gartley bi-patterns. Folks, the Gartley bi-pattern is in a market that's moving higher. You get an A to B equal CD to the downside, and that's what we refer to as A. So it's the same thing as a buy the D point pattern. And so each of those formed a nice bull sash candles to confirm that pattern. So I'm showing the A to B equal CD patterns on my screen. People can see it's got a one, the one to one level. Then I go to different Fibonacci expansions. I use 1.272, 1.618, and the 2.0 level. And what folks need to understand is the way that I look at an A to B equal CD pattern to the upside or the downside, we're talking about the downside, the way that we know that the pattern is completed is the market will tell us and will tell us by forming some type of bullish reversal candle. And that's one of the tools that I teach to subscribers out there. So we've got weekly Gartley bi-patterns. It's really important for us to understand where the profile levels, where resistance areas are. So folks are looking at our screen or copying it. It's in the upper right-hand corner. It shows you top W, center W, bottom BOTW. That's the weekly chart. And it's just the center of the top and the bottom bottom is where the buyers are at. Top is where the sellers are at. Another support resistance to observe is what I refer to as the oscillator and change line. And we can clearly see that last week's move was really a test of that oscillator and change line, a test of resistance, especially if you look at the IWM out here. Big move last week, right? But ran boom, right smack dab into resistance out there. This is the weekly equity futures contracts. They each also form Gartley bi-patterns. So we've got really nice significant bi-patterns. However, the issue is, can price take out resistance? And so far, the answer is no, it hasn't. And so here, just like the Russell 2000, lower right, if you see it, folks, you can see it ran right up into that red oscillator and change to no. Red oscillator and change line is more of a problem than a green one. A red one tells us that we have a falling price oscillator blow zero, and that's a very bearish condition. So in the case here of both the Dow, which had an amazing rally last week, at the Russell 2000, they ran right up into resistance. How does that work? It's a beautiful thing. We take a look at the daily time frame here for the spy, the diamond, the IWM. They completed what's referred to as rogment to indicator bottoms, that cues a TD9 count bottom. And the cues here, the cues ran right into resistance. The breakdown level was at 369.92. Now that's using the TD9 count system out there. Just gives us an objective level of resistance. So we've run into resistance, resistance, resistance out there. That's important to understand. The point that I'm trying to make is that last week's rally, it's run into daily and weekly resistance areas. And therefore, at this moment in time, we do not have a clear signal of any kind of a market breakout. So for our resistance, the next logical question is that mean the market is topped? And the answer there is the market is most likely forming a short-term top. And what I look at here, this is the New York Stock Exchange. And the center panel here, it's as advanced client oscillator. That's where we're taking a look at. And what this did was this got into extreme overbought territory. And we'll get into the overbought territory. That's a move above the plus 150 level. That condition needs to be worked off. Now, the cool thing is, what I really think is gonna take place here now, the market's gonna form its next top and it's not right here right now. If you take a look at all these green diagonal lines up at the highs where price is moving higher, but then look down at the advanced client oscillator where it's moving lower, I believe whenever we get above this 150 area, and we were at the highest level since January of this year out there, that's typically the way that a top forms. So this is the pattern that I'll be looking at. And that's when I believe that we set the next top inside the markets. You know, it's so cool, Steve, but you're just in two. And folks, it is so hard to do a weekly Gartley. Oh, it is. I mean, this is, it's not easy, folks, okay? No doubt. Yeah, and my mind's still open to that. We could have an amazing project. Oh, no, no, I get it. I get it. It's just really cool, man. Well, listen, man, can you just text me to that guy's that- I will, absolutely. Awesome, man, awesome. Absolutely. Have a great one. Hey, have a great one. Have a safe one, Steve. Thank you, everybody. I think that if you want to be successful at trading in the stock market, you're going to need a crystal ball. After all, it's impossible to predict the future, right? Like any endeavor in life, before you decide it's impossible, get some advice from the experts. You might find that it's not so impossible after all. For daily market overviews that give you direction on the key indices, selective stocks, and commodities, subscribe to the opening call newsletter at tfnn.com. The opening call newsletter is written by Basil Chapman, creator of the trading methodology known as the Chapman Wave. The Chapman Wave up-down sequence gives you an edge in identifying price turns, finding the peaks and valleys in stock prices.  First-time subscribers also get a 30-day money-back guarantee. If you're not satisfied, let us know, and you'll get a full refund within 30 days of signing up. tfnn.com, Educating Investors. Steve Rhodes started his trading career as a student almost 20 years ago, and the student has now become the master. Steve won the prestigious Timer of the Year award in 2018 and barely missed that mark again in 2019, finishing it number two for the year, an amazing accomplishment. 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Let's go and take a look at the spy because I want to show you that, when markets are moving like this folks, okay? So here's a, as Steve was just talking about, we're at resistance just about everywhere, right? But it totally makes sense too because watch what happens here. When you move as fast as we did last week, in six days, the bottom line is that, we can say that it already came back to August 15th, but that's pretty intense, okay? Because we're at November 3rd and 4th, right? So what tends to happen is this, this is what you like to see, which we have in the spy. So as you go up, you see that the type of volume that we have at the highs, most times what happens if you are gonna basically give it up on spades, meaning you're not gonna be able to get through resistance is that as you go higher, you'd have a contraction of volume. Now we don't have that. We have an expansion of volume as you go higher, but it's just like an elastic or anything else. That is quite a move and you're up to the next level. So the bottom line is that when you go south, what does happen is this. As you're going up to the next level, this down the bottom is the volume, you would see that drop off dramatically. Now that's not what we have. What we have is that you have volume on the move. Now this is gonna get choppy, it can definitely get choppy. Now someone had brought this up in the den last week and this was a great question and I didn't get the answer last week. What the question is, is this a three-gap play? So watch this, one, two, three. There's three gaps, right? So let's go through and get three-gap play because I've paid many tuitions, meaning I didn't lose money. I paid tuitions for my kids when they were in school on three-gap plays because they're really cool things to trade. So the way a three-gap play works is this. As you have an expansion on the upside and you can see this is a beautiful three-gap play and what happens is the reason I'm saying it's a beautiful one, the first one's a smaller one, the next one lodged and the next one's lodged. If in fact this is a three-gap play, what we'll end up seeing is this. You'd go sideways for a bit, then all of a sudden you gap down once. You don't have to gap down, you just come down. You go around on the second one, you get down on the third one. Now if that's what we do folks, okay, and we do it with light volume, you wanna be ready to buy hand over fist, okay? Because the way a three-gap play works is this. Wherever the gaps are in the first place, that's the trend. And in this particular case, of course, the gaps are upside. If in fact we get back down there, you guess what? You just, if you play options, go right in the option market, man, because these things, when they operate, man, they operate in spades. So we'll see if that's what we get. You know, it's possible, that's for sure. It would take quite a bit, meaning inside the bond market for us to basically come back down at this point and nail those gaps. Because what we do have, as I said a little bit earlier, you have a huge, you still have a huge amount of shots inside the note and bond market. You know, see, this is a, we're at a dynamic turning point here, and we'll find out whether the bulls are gonna be right or the bears are gonna be right inside the bond market. Mostly right now, you still have bears inside the bond market, and what that means specifically is that you go to lower price, higher yield. Bottom line, we'll see how this shakes out. Right now, we came off those lows, you came off them with volume. You're pulling back today with lighter volume. If we go look at the TLT, what you're gonna see is the same type of setup. Now the TLT is the 20 year plus, and you're gonna see that bottom line is down to 84 cents.  And today you're back in town with 32. That's what you'd love to see. Now what happens in the TLT, this just turn around and not fill the gap, but there's a gap right below us, that absolutely can get filled. We'll sell that shakes out. If I go over to the 10 year and take a look at the 10 year, what you're gonna see in the 10 year is that it took like a couple weeks for it to get off the low. You had 1.4 million, you're going at the 2.8 million. That being said though, bottom line is that, yeah, do it this way. Right there is game. You can come all the way back down there easy because that's just how markets go. They move higher. If a market wants to go higher, they're gonna move higher with volume. They pull back with lighter volume, and they'll pull right into the last place where we broke out from. And that's where we broke out from was the 105, 27th and 10706. So inside, let's go inside the Dow industrials and take a look at the Dow industrials, the strength versus the weakness inside the Dow out here. Okay, so point wise out here today, whoops, there we go, point wise out here today, we have United Health putting 22 positive points, Amgen 21, Microsoft 18, Apple 15, taking away from it, Goldman, minus 24, Caterpillar minus 18, let's go to Goldman. Goldman, that's G.S. Goldman had quite a run on Friday. And I don't know if that had to do with they, yeah, that didn't have quite a run. I mean, Goldman in six days went from, what is it? It's not much, that's quite a run, 250 to 324. Now that's a run. And I suspect what that's probably all about is that they actually made less partnerships this year than they have in a long period of time. You can see that side of strength. That's a huge side of strength. In Goldman's case, and let's see if we go this way. All is this, well, not all is it. It actually has another, this is interesting for the banks. See, this hasn't broke, even though we had that side of strength, this hasn't broken its downtrend yet. It's right up against that channel line. So let's go look at J.P. Morgan. Let's see where these babies sitting up. Same deal, yeah, yeah. See, these banks are still, yeah, these banks are still having a hard time catching price. Now what will happen, this is what gets wild. So picture, if we remember when Silicon National Bank went down, right? The bottom line, they were down because they bought way too many treasuries at too high a price. So the bottom line is that they're illiquid, they're underwater. Now when that happened, the Federal Reserve decided to change the rules inside the context of your bank's balance sheets, and they decided that even if you were in a loss, that you didn't have to register the loss against the amount of funds that you needed to stay in business. So in the context of rates coming down, this is where it's gonna get intriguing because the banks will basically start getting more capital on the way up. Now they got a long way to go, man. They got a long way to go, but it is intriguing all the time when you change the roof for one thing and then all of a sudden it goes back up and guess what, wouldn't we all love that, that we have a trade that goes bad? Somehow it says that, oh, you don't have to worry about it going bad, you don't have to pay anything. We'll just wait for it to go good. Well, next lifetime, folks, maybe you'd be a banker. Stay right there, folks, come right back. Tires, every Tuesday and Thursday, Tim Ord joins the Tom O'Brien show to share his unique insight that he's developed over decades of trading. Now, on Tuesday, November 7th, from 4 p.m. to 5.30 p.m. Eastern time, Tim Ord will be hosting his own live webinar. Tim's analysis has been outperforming market returns by almost double and his gold analysis is on track to be a winner as well. Tim will be delving into six secret ratios that every trader should know. In this webinar, Tim will be covering the Daily TLT VIX, the Daily and Weekly SPI VIX, the American Association of Individual Investors Bull Bear Ratios, and the Trin Panic Levels. Tim will break down each ratio, how it is calculated, its importance, and how it can help you make bigger returns. It's as simple as this. Learn the ratios, trade by them, and see your returns. That's it. Visit the front page of tfnn.com today to sign up now. T-F-N-N, educating investors. If you're looking for potential trading setups in the stock market, then Rocket Equities and Options Report is a newsletter you should try. Tommy O'Brien delivers options and equity trades when the markets present them, using a combination of fundamentals and technicals. Sign up for Rocket Equities and Options Report today with a 30-day money-back guarantee so you have nothing to risk. For all the details and to start your subscription today, visit the front page of tfnn.com. T-F-N-N, educating investors. 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TFNN has been educating traders for more than 20 years with live programming hosted by a variety of professional traders during market hours. The Tiger's Den, available to all tigers and tigeresses for just $1 for the year. There's no catch or added costs when you join our community of traders. Sign up today and become a part of this educational community of traders. Just visit the front page of TFNN.com. This program is brought to you by Vista Gold, printed on the NYSE American and TSX under the symbol VGZ. Welcome back, folks. Let's get over to that oil market and take a look at oil. So oil's been bouncing around in a monster way. It's hard to comprehend sometimes that we, oil runs the whole world and oil can trade every day within like $2. So what we have out here today is that you're up 42 cents, but you've rejected higher price at $82.24. So I suspect what we're gonna see here is it's gonna try to break down like the bond market broke down. It's been trying to, well, it has been going into these lows now for five days. We came down hard on Friday, we had it didn't break it, just broke it a bit. So there is, we have, right there, I mean, there's a lot of support at this level. That being said, it looks to me like this oil market actually wants to go to $71.99, wants to go all the way down to this level here. So it's in a dangerous spot right now. We'll see how this shakes out in the next couple of days. If we go to the XLE, and we take a look at the XLE, same type of setup. Yeah. So in the XLE, you can see that we caught a bid Thursday Friday, which it should, because the market was up so dramatically, okay? Bottom line is not holding the bid, and it's doing the exact same type of deal, meaning it's coming into the lower end of this consolidation that it's been in. Now the difference with the XLE is that, yeah, we're at 85, and the pullback would be 80, 42. We go to XOM, because Sharon and Exxon, those are the two largest weightings, and they both, you know, it's always a while like this. They both turned around and did a big buy, meaning buy in another company. And they did it because of course oil's been so high, and they've been making so much money, and that's what tends to happen to all these companies, man, and then all of a sudden it pulls back. I mean, I remember the gold market in 2011, everyone was buying everyone, and that was the end of the market for like five years. So if we take a look at Exxon Mobile, that's at 106, where you can see the bottom of this consolidation. Now the bottom of the consolidation on Exxon Mobile is there's a lot of strength, man. There's a lot of support, because you can see going back six months we've traded there, and then let me see this on a weekly. Yeah, see on a weekly, to me, this still has a high volume low, and it's gonna go after it, yeah. On a weekly, yeah, we're at 105, 96 is gonna be very dangerous. You know, we came down there before and the first time it was all the support that you have going all the way back to January, May through August of 2022. There's a lot of support there. We go look at Chevron. This is a different manumber, man. Chevron got hit hard, man. Look at this. So Chevron just went from 173 to 147. Now this is a whole different animal, man. What's going on here? Oh, Chevron already broke its consolidation. Interesting. Okay, so Chevron broke one consolidation. They're coming down to where it had some strength. We're gonna bring this back further. Yeah, the market didn't like that deal with Chevron was buying, that's for sure. Yeah, this could be a problem for Chevron. So that'd be a problem for the XLE, too. We're going back to the bottom of this whole consolidation, which in Chevron's case, gets you down to where 147 gets you to 137. That's quite a breakdown. What also happens here, you see how long this top was? That is a problem, man. You don't like to see big, long tops like this. In fact, watch this. I'm gonna open this up for you a little. Because what you're gonna be able to see is that all the volume on this top is at the lowest. First, hit the breakout. Then we made a high with 44 million. You go south with 90 million. You make a high with 39 million. You go south with 22 million. And then we just went south with 79 million. If you have the out of time in the trade, this is a classic, man. Up at the highs, no volume. All the lows volume, that's building costs to break down. That's how that's shaking out. So that's a heads up in spades, man. That's also, we'll see what that's like. Let's go to COPPA HG. That's what we're going through these. COPPA active contract, okay. So on COPPA, we're laying out at 371 a pound, HG1. Let me do a generic one on this. See how far I gotta go back. Put that. Okay, let's see what's happening here. So what COPPA we did is this. You come off the high of five bucks. You get down to 315. You're 371 right now. Yeah, this has to build costs and how to get through this monster down draft that we had out there from the 407 to the 315 area. But this looks to me like COPPA does want to make this run again to the 435 area. If we go take a look at a couple of the COPPA stocks, SCCO wasn't moving too much. Yeah, it's hanging tough there. It's building costs, but it's not moving that much. TGB, which is to say go. This looks like it wants higher price. Now I tried higher price stage, it didn't have enough volume, but to say go looks like to me like you gotta get a high swing point out here of 160. You put this on a, yeah. So that came off the bottom with conviction. When they come off the bottom of conviction, they're going right back to the highs, man. Not right back to the highs, but you can see you get volume up here at the 160. Then we also, yeah, you gotta take it step by step. It's gonna be the 160 on that baby on the way up. Now a lot of this is gonna be predicated also on the dollar because what you will see, and this will get intriguing inside the oil market because now oil pullbacks, this is a double bag, oil pullback and the dollar pullback. So you can see that other countries how inexpensive it was last week, compared to it was the prior week because you had two different things that ended up happening. The dollar went down in a big way. Oil went down in a big way. Oil's priced in New York's dollars. Dow, Dow Industries right now, Dow and One Nasdaq is up 19, S&P's down one, stay right there folks, come right back. Are you ready to take your trading to the next level? Introducing Tom O'Brien's award-winning newsletter, Market Insights. Your key to successful active trading. Tom O'Brien, renowned for his expertise in the financial markets, has designed Market Insights to be your daily guide to profitable trades. Tom publishes his daily Market Insights newsletter every market day before the market open, along with updates when warranted. Stay ahead of the game with Tom's real-time analysis and trade recommendations delivered straight to your inbox.  Ready to join the ranks of successful traders? Head over to TFNN.com and subscribe to Market Insights today. Don't miss out on this opportunity to supercharge your trading results. Market Insights comes with a 30-day money-back guarantee for all new subscribers, so you have nothing to risk. Don't miss out on this opportunity to revolutionize your trading game. Head over to TFNN.com right now to join thousands of traders who have already experienced the power of Tom O'Brien's award-winning newsletter, Market Insights firsthand. TFNN, educating investors. You might think that if you want to be successful at trading in the stock market, you're going to need a crystal ball. After all, it's impossible to predict the future, right? Like any endeavor in life, before you decide it's impossible, get some advice from the experts. You might find that it's not so impossible after all. For daily market overviews that give you direction on the key indices, selective stocks, and commodities, subscribe to the opening call newsletter at TFNN.com. The opening call newsletter is written by Basil Chapman, creator of the trading methodology known as the Chapman Wave. The Chapman Wave up-down sequence gives you an edge in identifying price turns, finding the peaks and valleys in stock prices.  First-time subscribers also get a 30-day money-back guarantee. If you're not satisfied, let us know and you'll get a full refund within 30 days of signing up. TFNN.com, educating investors. Everything in the universe is governed by the Fibonacci sequence. This mathematical principle is responsible for everything, from the most aesthetically pleasing artwork to patterns in the stock market. To stay on top of stock patterns you can take advantage of, sign up for the Fibonacci 24-7 newsletter at TFNN.com. When you subscribe, you'll get a weekly report from Veteran Day Trader Larry Pezzavento on stocks you need to pay attention to, and you can trust Larry's analysis. After all, he's got 45 years' experience as a day trader. Larry will also provide daily charts, videos, and data on the key markets that he's tracking. Expect notifications from Larry on market movement you need to act on at any time. First-time subscribers also get a 30-day money-back guarantee. If you're not satisfied, let us know and you'll get a full refund within 30 days of signing up. Subscribe to the Fibonacci 24-7 newsletter today. TFNN.com, educating investors. Don't forget, you can listen to TFNN live on your mobile device 24 hours per day. Go to TFNN.com and hit Watch Tiger TV. That's TFNN.com and hit Watch Tiger TV. Welcome back, folks. Open AI, so this is gonna get really interesting, folks. Open AI is now letting users build custom versions of ChatGBT to accomplish specific, personal and professional tasks as the artificial intelligence startup works to beat competition back now. So check this out. With a new option used, we'll be able to quickly create their own specialized versions of ChatGBT that can help teach math to a child, explain rules of a board game, the company said on Monday, now here's the kicker. No coding is required, the company said. Now here's the real kicker. Open AI also plans to introduce a store later this month where users can find tailored GPTs, that's what they call them, from other users and make money from their own, much as they might with apps in the Apple App Store.  Check it out. That looks to me like it's gonna be quite an opportunity that you can get really creative and you can actually get creative on ChatGBT in order to make a program that you can put in the store at ChatGBT that may make you some bread. So this is moving fast, folks, okay? This is moving real fast. Now the coolest thing for someone like me, if you know nothing about coding, you can have a lot of good ideas, you can ask a lot of questions and we all have a lot of different ideas about what we'd like to see. So that looks to me like that company store, they just might, yeah, they will explode, because there's gonna be, and that's considered middleware then, folks, that's what ends up happening. You have the actual, the ChatGBT on the cloud, the middleware and then the end user. Always remember, folks, the bank and Chloe will hide out the book and run you over and thank God, there's always another trade. Health, abbeys, and prosperity. Have a great night, folks. Have a safe night. Come back and visit Tommy tomorrow morning, kicks us off 9 a.m., great show, folks. Yeah, look at him, folks.


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