Increased oxidative stress has been previously shown to compromise insulin signaling via several ways including but not limited to, activation of the NF-κB pathway via the phosphorylation of its inhibitory subunit, IκB, by the serine kinase IKK, disruption of the intracellular distribution of PI3K, activation of serine/threonine kinases which then phosphorylate the serine/threonine residues of components of the insulin signaling pathway such as the Insulin Receptor and Insulin Receptor Substrate elevating the risk of insulin resistance and diabetes mellitus [47,48]. This evidence concerns the gene NFKB1 and Insulin resistance.