The majority of advanced prostate cancers respond to ADT, but they inevitably progress from castration-sensitive prostate cancer (CSPC) to castration-resistant prostate cancer (CRPC), which is driven by a range of androgen receptor (AR)-dependent and independent mechanisms (e.g., AR amplification and neuroendocrine trans-differentiation, respectively) [12]. The gene discussed is AR; the disease is prostate carcinoma.