Approximately 80–90% of patients with the metastatic disease showed quite proper clinical and biochemical responses achieving a rapid decline in serum prostate-specific antigen (PSA) at the beginning of endocrine therapy (Amaral et al., 2012) and depletion of serum testosterone to “castrate” levels (<50 ng/ml), resulting in induction of apoptosis signaling in malignant prostate cells and temporal suppression of disease (Kahn et al., 2014). This evidence concerns the gene KLK3 and metastatic neoplasm.