The array of proinflammatory mediators, such as cytokines, adipokines (e.g., leptins), lipocalin-1, serum amyloid A-3, and adiponectin released during the development of obesity-related chronic inflammatory phenotypes promote insulin resistance by altering the extracellular matrix, the capillary network architecture, and the glucose uptake mechanisms [102]. The gene discussed is INS; the disease is Obesity.