AR and posterior cortical atrophy: Several mechanisms causing progression to CRPC have been described: (1) AR gene amplification and overexpression; (2) somatic AR mutations; (3) prostate intracrine androgen biosynthesis; (4) AR splice variants (AR-Vs); (5) non-canonical AR transactivation; (6) AR-independent bypass pathways; (7) AR-negative cell populations: PCa stem-like cells; and (8) AR-negative cell populations: neuroendocrine PCa cells and other subtypes [10].