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Nuclear factor κ-light-chain-enhancer of activated B cells (NF-κB) is a sophisticated transcription factor that is particularly important in the inflammatory response, but it regulates more than 400 individual and dependent genes for parts of the apoptotic, angiogenic, and proliferative, differentiative, and cell adhesion pathways. NF-κB function is directly inhibited by the binding of inhibitor of κB (IκB), and the imbalance between NF-κB and IκB has been linked to the development and progression of cancer and a variety of inflammatory disorders. These observations might broaden the horizon of current knowledge, particularly on the pathogenesis of inflammatory diseases considering the roles of NF-κB and IκB. In this context, we focus this narrative review on a comparative discussion of our findings with other literature regarding variations of  NFKB1  and  NFKB1A  and their association with susceptibility to widespread inflammatory disorders (such as atherosclerosis, morbid obesity, Behçet syndrome, Graves disease, Hashimoto disease) and common cancers (such as gliomas).

Functional variations of NFKB1 and NFKB1A in inflammatory disorders and their implication for therapeutic approaches