This biphasic behavior of β cells is not fully understood but appears to be a universal phenomenon seen not only in type 2 diabetes but also in congenital hyperinsulinism (59, –, 61) and in different rodent models such as leptin receptor deficient mice (db/db), (62), β cell-specific deletion of TSC2 in mice (39), and Psammomys obesus exposed to a high calorie diet (63). Here, TSC2 is linked to hyperinsulinism.