In the mouse, Ins2 is predominantly transcribed in the thymus, while Ins1 expression is dominant in islet β cells, which leads to a higher immunological tolerance to Ins2. This explains why the breeding of Ins2−/− mice onto the NOD background accelerates insulitis and diabetes onset (34), whereas insulitis and diabetes are markedly inhibited in Ins1−/− congenic NOD mice (35). Here, FOXM1 is linked to diabetes mellitus.