The activation of the NF-κB signaling pathway by some stimuli, such as inflammatory agents, carcinogens, tumor promoters, viral proteins, stress, chemotherapeutic agents, and γ radiation results in the phosphorylation of the IκB subunit by activated IKKs, leading to the proteasome-mediated degradation of IκBs. This evidence concerns the gene NFKB1 and neoplasm.