Upon prolonged treatment with ADTs, a subset of PCa becomes resistant to this treatment [castration-resistant prostate cancer (CRPC)]; however, AR signaling continues irrespective of non-response to ADTs by various means, including gain-of-function mutations in ARs, copy number variations of ARs, mutations in co-repressors or co-activators of ARs, and others [11,12]. The gene discussed is AR; the disease is posterior cortical atrophy.