Ever since Cerasi and Luft have recognized that type 2 diabetes (T2D) is caused by the relative inability of β cells to secrete sufficient amounts of insulin to compensate for insulin resistance, and not by insulin resistance itself (1), underlying mechanisms of this β-cell defect have been searched for and found quite complex, with β-cell inflammation as a major factor in both T1D (2) and T2D (3, 4). This evidence concerns the gene INS and type 1 diabetes mellitus.