The molecular mechanisms behind inflammation-induced insulin resistance in the adipose tissue mainly rely on the findings that inflammatory cytokines, specifically TNFα, can activate c-Jun NH2-terminal kinase (JNK) and IKK serine-kinases, which promote the inhibitory phosphorylation of IRS1 on Ser307, leading to the disruption of insulin receptor signaling (30). This evidence concerns the gene INSR and Insulin resistance.