In our previous studies, we showed that CDK5 regulates the apoptosis and proliferation of prostate cancer cells [3,53,77], and that RA treated prostate cancer cells may either induce p35 cleavage into p25 to result in overactive CDK5 activity in a high dose treatment [3] or upregulate CDK5 expression as well as subsequent p27 expression in a low dose treatment [77]. The gene discussed is CDK5; the disease is prostate carcinoma.