Despite frequent and durable responses of ARPI in advanced prostate cancer (PCa), progression to castration‐resistant prostate cancer (CRPC) inevitably recurs, most often driven by AR reactivation involving genomic alterations, cross‐talk signaling with kinase pathways, and coordinated action of different stress pathways (Wyatt & Gleave, 2015). The gene discussed is AR; the disease is posterior cortical atrophy.