Oxidative stress is believed to lead to the activation of inflammatory processes that could further contribute to the development of insulin resistance through inflammatory cells [4] or via activation of stress-kinases (e.g., JNK), which could lead to the serine/threonine (Ser/Thr) phosphorylation of IRS-1 and IRS-2 and in this way impair insulin signaling [54]. The gene discussed is IRS1; the disease is Insulin resistance.