TNF-α-induced NF-kB activation seems to play a major role during these pathophysiologic circumstances as well [51]; upregulated NF-kB transcription might be a critical link between inflammation and cancer, as inactivation of the NF-kB pathway attenuates the formation of inflammation-associated tumors in a colitis-associated cancer model in mice [52]. The gene discussed is NFKB1; the disease is cancer.