The mechanism underlying the increase in CRPC risk for patients with steep PSA decline remains largely unknown, but postulated theories suggest that it is a result of the transcriptional effect of ADT on PSA production rather than prostate cancer cell death [16]; rapid removal of hormone-sensitive prostate cancer cells inducing an adequate environment for the growth of hormone-resistant prostate cancer cells [9]; or high probability of these subsets of patients containing cancers with low PSA production, such as cells with neuroendocrine differentiation [10] or cancer stem cells [17]. This evidence concerns the gene KLK3 and Familial prostate cancer.