However, in many types of cancer, NF-κB is constitutively activated and induces expression of genes that promote cancer cell proliferation, invasion, angiogenesis and apoptotic resistance [11], suggesting that in cancers, either the proinflammatory mediators are aberrantly elevated and override the negative feedback control and/or mechanisms to terminate NF-κB activity are defective, thus enabling NF-κB to promote tumorigenesis. Here, NFKB1 is linked to cancer.