Activated the inhibitor of NF-κB kinase (IKK), caused by cytokines, hyperglycemia and elevated free fatty acids (FFAs), results in the nuclear factor of kappa light polypeptide gene enhancer in B-cells inhibitor, alpha (IκBα) polyubiquitination and proteosomal degradation, and subsequent release of NFκB, especially p50/p65, to the nucleus where it can bind to the response element of target genes involved in the inflammatory response [14-16]. The gene discussed is NFKB1; the disease is Hyperglycemia.