In this study we screened a panel of replicating mutants with small E1A-deletions previously demonstrated to be defective in binding to pRb (dl1108, dl922–947), p300 and p400 (dl1101), p300/CBP (dl1104), and p400 and p21 (dl1102) [24], [31], [35], [36], [37], to explore whether the specific E1A gene regions that bind to these and other cellular factors are essential for sensitization to drugs currently used in the clinic for prostate cancer: mitoxantrone, a topoisomerase inhibitor, and docetaxel, a microtubule-interfering drug. The gene discussed is EP300; the disease is Familial prostate cancer.