Autoimmune destruction of insulin-producing cells underlies the pathophysiology of type 1 diabetes (T1D) [1], whereas chronic metabolic stress linked to obesity and insulin resistance results in a gradual impairment of pancreatic function, demise of β-cells, and ultimately causes type 2 diabetes (T2D) [2, 3]. This evidence concerns the gene INS and obesity due to melanocortin 4 receptor deficiency.