The current view on the persistent and reactivated AR signaling in CRPC, that forms the basis of targeting the AR-axis signaling in ADT, is largely based on the facts of positive AR expression detected in clinical CRPC tumor tissues [11, 41], persistent AR activity and intraprostatic androgen levels in primary prostate tumors from androgen deprivation-treated patients [42], recurrent serum PSA levels and also the persistent AR activity as shown in experimental xenograft models of CRPC [43–47]. This evidence concerns the gene AR and prostate neoplasm.