Inflammatory cytokines such as TNF-α or interleukine-6 (IL-6) induce insulin resistance via the activation of serine/threonine kinases such as Jun N-terminal kinase (JNK), nuclear factor-kappa B (NF-κB), and mammalian target of rapamycin (mTOR) that promote inhibitory serine phosphorylation of IRS-1 (insulin receptor substrate 1). This evidence concerns the gene MARK2 and Insulin resistance.