At the molecular level, several mechanisms linking the activation of inflammatory pathways and impaired insulin action come into play: activation of IκB kinase complex, extracellular signal-regulated protein kinases 1 and 2 (ERK1/2), and c-Jun N-terminal kinases (JNKs) in inflammatory tissues in individuals with obesity decreases tyrosine phosphorylation of the insulin receptor substrate (IRS) proteins, leading to an attenuation of insulin signaling [27]. The gene discussed is INS; the disease is obesity disorder.