Canonical NF-κB activation by PRRs, and other diverse ligands such as cytokines, leads to degradation of inhibitory proteins (such as IκB) and release of NF-κB TF dimers, predominantly p50 and p65 (RelA), which translocate into the nucleus to upregulate an array of genes that govern cell-autonomous and adaptive responses against infection [1, 6, 7]. This evidence concerns the gene NFKB1 and infection.