 This antiandrogen resistance may also be linked to the relative weakness of current antiandrogens as they have an affinity 50 times or more lower than that of DHT for the AR.This may also explain why compensatory AR overexpression is often observed.AR gene mutations in the LBD that alter ligand specificity and/or functional activity exist and are thought to contribute to the conversion of some AR antagonists into agonists, which explains the paradoxical temporary improvement sometimes observed in patients when antiandrogen therapy is stopped.