Using LNCaP, LAPC4 and CWR22Rv1 PCa cells, a cyclic proteasome-dependent degradation of AR during G1 was observed, along with co-immunoprecipitation (co-IP) of AR with replication complexes (RC), and co-IP of AR with origin of replication complex 2 (ORC2) in four of seven human CRPC metastases, suggesting AR may function as a licensing factor for DNA replication in cells that are androgen-sensitive for growth. This evidence concerns the gene AR and posterior cortical atrophy.