As our results demonstrate that MEM treatment induced apoptosis and cell cycle arrest by modulation of TPD52 expression in both PCa cell lines (CWR22Rν1 and C4-2 cells) shown earlier by cleavage of Caspase 3 and PARP, also by modulation of cyclin-dependent kinases in CWR22Rν1 and C4-2 cells by treatment of MEM in a dose-dependent fashion. The gene discussed is CASP3; the disease is posterior cortical atrophy.