Prostate cancer pathogenesis is dependent on oncogenic activation of androgen receptor (AR) signaling by testosterone and the more potent 5α-reduced metabolite, 5α-dihydrotestosterone (DHT).1 Although patients are usually responsive to ADT initially, a subset of patients develop castration-resistant prostate cancer (CRPC) with poor prognosis. The gene discussed is AR; the disease is Familial prostate cancer.