IRS1 and Insulin resistance: Another mechanism by which insulin resistance can occur involves another inflammatory kinase IKK-β, which through direct serine phosphorylation of IRS-1 and phosphorylation of the NF-Κβ inhibitor induces the production of several inflammatory mediators, including TNFα and IL-6, which inhibits serine phosphorylation of IRS-1 and thus the translocation of the glucose transporter (GLUT 4) [35, 43].