Given the significance of both AR and p16Ink4a alterations in human prostate cancers, we developed R26hARL/wt:p16L/L:PB-Cre4 compound mice in which the deletion of the p16Ink4a gene and conditional expression of the human AR transgene co-occur in the prostatic luminal epithelium. The gene discussed is CDKN2A; the disease is Familial prostate cancer.