The progression of PCa to castration-resistant prostate cancer (CRPC) is frequently driven by somatic alterations in the phosphoinositide 3-kinase (PI3K)/protein kinase B (AKT)/mammalian target of rapamycin (mTOR) pathway, indicating that therapies targeting this pathway could improve survival outcomes and therapeutic efficacy. The gene discussed is MTOR; the disease is posterior cortical atrophy.