In general, as no loss-of-function mutations of the inhibitory subunit IκB or gain-of-function IκB kinase mutations have been detected, it has been suggested that NF-κB activation in cancer may be the result of either exposure to proinflammatory stimuli in the tumor microenvironment or mutational activation of upstream components in IκK - NF-κB signaling pathways [25]. This evidence concerns the gene NFKB1 and neoplasm.