While the pathophysiologic mechanisms by which systemic inflammation leads to increased risk of MetS are not clearly evident, both adipokines produced in hypertrophic adipocytes [10] and production of pro-inflammatory cytokines such as TNF-α, IL-6, and monocyte chemoattractant protein-1 released from adipose tissue of increased infiltration by macrophages may play an important role in the pathogenesis of MetS [33, 34]. The gene discussed is IL6; the disease is metabolic syndrome.