Consistent with the resistance of CaP cells to clinically relevant doses of TNF-α, this cytokine was shown to increase NFκB signaling and increase expression of c-FLIP, cIAP-1 and Bcl-2, three known NFκB-regulated anti-apoptotic targets in prostate cancer cells (30, 31). The gene discussed is BCL2; the disease is Familial prostate cancer.