Numerous lines of investigation suggest that nuclear factor NF-κB, a proinflammatory transcription factor, could promote tumorigenesis. Various inflammatory agents, carcinogens, tumor promoters, and the tumor microenvironment activate NF-κB. NF-κB proteins themselves and proteins regulated by it have been linked to cellular transformation, proliferation, apoptosis suppression, invasion, angiogenesis, and metastasis. Constitutively activated NF-κB is common in wide variety of tumors. Furthermore, there exists genetic evidence that NF-κB mediates tumorigenesis. Thus, suppression of NF-κB activation should be effective in the prevention and treatment of cancer.