Dysregulated NF-κB activity facilitates immune escape, proliferation, and neovascularization mediated by numerous target genes, proteins, and inflammatory modulators such as tumor necrosis factor α (TNFα), vascular endothelial growth factor (VEGF), COX-2, and a broad array of interleukins (IL), cytokines, and chemokines, thereby driving tumor aggressiveness [24,25]. Here, NFKB1 is linked to neoplasm.