Notably, specific AR mutations are frequently discovered after the emergence of therapeutic resistance and may change the ligand binding affinity and alter the prostate cancer response to AR inhibitors (ARIs) [9, 13], resulting in constitutive activation of the AR pathway and progression to castration-resistant prostate cancer (CRPC), which is the final stage and a lethal form of PCa [13, 14]. The gene discussed is AR; the disease is posterior cortical atrophy.