To test the hypothesis that combinatorial repression of HDAC1/2 and PI3K/AKT signaling would effectively inhibit the growth of both ARPC and NEPC phenotypes, we determined dose–response effects of the dual HDAC/PI3K inhibitor fimepinostat on the growth and cell viability of a broad panel of human prostate cancer and benign prostate epithelial cell lines. The gene discussed is HDAC1; the disease is prostate carcinoma.