AR and posterior cortical atrophy: Numerous studies utilizing PCa models with endogenously expressed AR, as well as cell models with exogenously driven increases in AR, have shown that increased AR expression and/or ligand driven activation may result in growth inhibition, variably attributed to cell cycle arrest in G1/S or the subG0/G1 phase, and/or frank DNA fragmentation and apoptosis [18,36,70,72,73,74,75,76,77].