Patients who failed ADT develop resistance through several different proposed mechanisms, including overexpression of either AR [21] or coactivators [22] which sensitize the AR to lower physiological levels of androgen; point mutations which can cause the AR to be promiscuously activated by relatively abundant nonandrogenic steroids; activation/sensitization of the AR through phosphorylation of the protein [23]; and interestingly intracellular de novo production of androgen by the tumor itself [24]. Here, AR is linked to neoplasm.