The resulting shift from an anti-inflammatory (lean) to a proinflammatory (obese) phenotype is coupled with a significant local and systemic increase in some of these key cytokines, including interleukin 6 (IL-6), IL-1, IL-8, and tumor necrosis factor α (TNF-α), which critically contribute to insulin resistance development [9]. The gene discussed is IL6; the disease is Insulin resistance.