Hypothalamic insulin resistance may be evoked by inflammatory stimuli [14,15] via the activation of intracellular proinflammatory pathways that increase the expression of intermediate proteins like Jun NH2-terminal kinase (JNK), protein tyrosine phosphatase 1B (PTP1B), inhibitor of nuclear factor kappa kinase (IKK), and endoplasmic reticulum stress [16,17,18,19]. This evidence concerns the gene MAPK8 and Insulin resistance.