Perhaps one of the greatest contributions of oxidative stress to insulin resistance is that it generates metabolites that create positive feedback loops for potentiation of TLR4, RAGE, and other signaling pathways associated with activation of NF-κB and insulin signal-inhibiting serine kinases such as PKC, IKK, JNK, and p38 MAPK. The gene discussed is TLR4; the disease is Insulin resistance.