A good example of this is the RelA-dependent anti-apoptotic effects seen following treatment with inflammatory stimuli, such as tumor necrosis factor (TNF)-α that contrast with pro-apoptotic effects following treatment with some DNA damage agents.9, 10, 11, 12, 13, 14 Understanding the mechanistic basis for these contrasting effects has important implications for the role of NF-κB in tumorigenesis and the response to cancer therapies.4 Here, NFKB1 is linked to cancer.