Overall, the results of this study indicate that small molecule inhibitor of the interaction of AR and p52 NF-κB subunit, AR/p52-02, represses castration-resistant prostate cancer cell growth by blocking both AR and p52 pathways, and shows promise for development of a new therapeutic agent for castration-resistant prostate cancer. The gene discussed is NFKB2; the disease is Familial prostate cancer.