NF-κB-activating stimuli such as bacterial infection, proinflammatory cytokines or LPS, facilitate IκB kinase (IKK)-mediated IκB phosphorylation and subsequent degradation of IκB by the proteasome machinery [20], resulting in the release and subsequent nuclear translocation of the NF-κB complex for regulation of genes that are involved in the immunity process, adhesion molecules and cell survival [21]. Here, NFKB1 is linked to bacterial infectious disease.