NFKBIA是抑癌基因，编码蛋白(NF-κB inhibitor α)是一种抑制NF-κB信号传递的蛋白，是一种由表皮生长因子受体（EGFR）通路激活的转录因子家族。NFκBIα通过提供NFκB 与细胞质中的抑制分子相互作用，来维持NFκB 失活状态。一系列外部刺激，包括促炎性细胞因子、生长因子或压力，可导致NFκBIα的磷酸化，随后导致NFκB的释放和核转位；进而导致数百个基因的转录的激活，这些基因参与调节免疫应答，防止凋亡和对外胚层组织形成至关重要的信号传导。NFκB 的缺乏经常是因为一个等位基因的功能缺失突变（小插入，缺失或错义）以及伴随另一个等位基因的缺失或失活。NF-κB信号传导的组成型表达导致编码抗凋亡蛋白和生长促进蛋白靶基因的过表达。NFκBIA的缺失具有与胶质母细胞瘤（GBM）中EGFR扩增类似的作用，并且与相对降低的存活率相关。此外，单核苷酸多态性和NFκBIA突变富集已在霍奇金淋巴瘤，结肠直肠癌，黑素瘤，肝细胞癌，乳腺癌和多发性骨髓瘤等癌种中发现。

The NFκBIα (NF-κB inhibitor α) gene encodes a protein that represses signaling of NF-κB, a family of transcription factors activated by the epidermal growth factor receptor (EGFR) pathway. NFκBIα helps keep NFκB in an inactive state by supporting its interaction with inhibitory molecules in the cell cytoplasm. A range of external stimuli, including pro-inflammatory cytokines, growth factors or stress, can lead to phosphorylation of NFκBIα and subsequently the release and nuclear translocation of NFκB; this results in the transcriptional activation of hundreds of genes that regulate the immune response, protect against apoptosis and signaling pathways critical to the formation of ectodermal tissues. Lack of NFκB is often due to loss-of-function mutations (small insertions, deletions, or missense) in one allele of NFκBIα coupled with deletion or inactivation of the second allele. Constitutive expression of NF-κB signaling results in overexpression of several target genes encoding anti-apoptotic proteins and growth-promoting proteins. Deletion of NFκBIA has demonstrated an effect similar to EGFR amplification in glioblastomas (GBM) and is associated with relatively reduced survival. Further, enrichment of single-nucleotide polymorphisms (SNPs) and mutations in NFκBIA have been observed in Hodgkin’s lymphoma, colorectal cancer, melanoma, hepatocellular carcinoma, breast cancer and multiple myeloma.

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