Further, MAOA was shown to be activated by relieving REST transcriptional suppression to inhibit apoptosis while activating autophagy to induce the neuroendocrine differentiation of LNCaP cells upon androgen deprivation (38), where acquisition of neuroendocrine features is an emerging mechanism enabling AR-driven prostate adenocarcinoma to evolve into AR-indifferent CRPC with resulting antiandrogen resistance (39, 40). The gene discussed is AR; the disease is prostate adenocarcinoma.