In CRPC, reactivation of AR pathways from multiple mechanisms occurs, including production of androgens by the adrenal glands and PCa cells themselves, androgen-independent activation of the AR, AR gene amplification or overexpression, constitutively active ligand-independent AR splice variants, and gain-of-function mutations involving the AR ligand-binding domain [12]. The gene discussed is AR; the disease is posterior cortical atrophy.