In addition to the epidemiological evidence establishing obesity as the leading risk factor for T2DM [4], the molecular mechanisms though which obesity contributes to the development of insulin resistance in insulin-responsive tissues (i.e., skeletal muscle, adipose tissue, and the liver) can be largely credited to the inability of mature white adipocytes to perpetually expand to accommodate excess energy in the form of triglycerides. The gene discussed is INS; the disease is obesity due to melanocortin 4 receptor deficiency.