Despite an initial therapeutic efficiency of 80–90% [2], several patients treated with ADT will develop castration-resistant prostate cancer [3], defined as castrate serum testosterone < 50 ng/dL or 1.7 nmol/L with either biochemical progression (three consecutive rises in PSA at least one week apart, resulting in two 50% increases over the nadir, and a PSA > 2 ng/mL) or radiological progression (either two or more new bone lesions on bone scan or a soft tissue lesion) [4]. The gene discussed is KLK3; the disease is prostate cancer.