In addition to AR-dependent metabolic alterations, the PCa-associated genetic aberrations that are not related to AR, such as p53 loss, phosphatidylinositol-3-kinase (PI3K) mutations, and loss of Phosphatase and tensin homolog (PTEN), also enhance lipid metabolism, exemplifying the close relationship between genetic drivers and metabolic reprogramming. The gene discussed is PTEN; the disease is posterior cortical atrophy.