A number of alterations involving different tissues have been found to contribute to the development and progression of hyperglycemia, and more relevantly, the progressive alterations of insulin, glucagon, and somatostatin production and secretion from the endocrine pancreas and insulin action in skeletal muscle, liver, and adipose tissue are the known hallmarks of prediabetes and T2DM [2–6]. The gene discussed is INS; the disease is Hyperglycemia.