Recently, several mechanisms have been proposed for the development of castration-resistant prostate cancer (3,4) including mutation, amplification (4,5), expression of alternative-splice variants (6), proteolytic removal of ligand-binding domain (LBD) (7) of the androgen receptor (AR), or the increase of natural testosterone biosynthesis by cancer cells (8,9). This evidence concerns the gene AR and Familial prostate cancer.