AR and cancer: It is now appreciated that in spite of castrate levels of androgens, the cancer cells are able to maintain persistent androgen receptor signaling through a variety of contributory mechanisms including AR gene amplification that results in overexpression of AR, gain-of-function mutations in AR which enable promiscuous activation of the receptor through other steroids or even in the absence of ligand binding, changes in AR co-activators and the expression of AR splice variants [6].