In T1D, hyperglycemia is caused by an immune-mediated destruction of pancreatic β-cells leading to an absolute deficiency of insulin production, whereas the pathogenetic mechanism underlying T2D involves a complex interplay between insulin-resistance and abnormalities in β-cells function, often due to pathologic obesity and dyslipidemia, and to other causes and factors, such as low-grade chronic systemic inflammation [4]. This evidence concerns the gene INS and obesity due to melanocortin 4 receptor deficiency.