Upon stimulation with a ligand such as tumor necrosis factor α (TNF-α) or lipopolysaccharide (LPS), IκBα is phosphorylated by the signalosome [39]; this phosphorylation induces the rapid degradation of IκBα, which determines the inhibition of NF-κB and leads to the translocation of p50/p65 into the nucleus to activate the transcription of downstream target genes, including cytokines, which promote tumor growth and invasiveness [39]. Here, NFKB1 is linked to neoplasm.