During infection, oxidative stress, or pro-inflammatory cytokine exposure, NF-κB is activated by transmembrane Toll-like receptors (TLRs) that are usually expressed in macrophages, and it plays an important role in recognizing immune-stimulating molecules and regulate the expression of inflammatory cytokines, including TNF-α, a hallmark of the cellular response leading to the activation of the innate immune system14,16. This evidence concerns the gene NFKB1 and infection.