Several clinical investigations have established a significant correlation between the onset of T2DM and several proinflammatory markers, including IL-6, IL-1β, and TNF-α.[34–36] Chronic exposure to high levels of glucose and lipids usually elicits countless pathways responsible for impaired insulin secretion from the β-cells, leading to a decrease in glucose utilization peripherally.[34]. The gene discussed is INS; the disease is type 2 diabetes mellitus.