The reduction in KATP-channels in MODY1 patients results in a flattening of the insulin-glucose secretion curve (41) so that insulin release is not appropriately stimulated at high glucose levels (hence, glucose intolerance and diabetes, as insulin requirements increase in MODY1 patients later in life), but is also not appropriately suppressed at low glucose levels (hence, hyperinsulinemic-hypoglycemia in early infancy in patients with HNF4A mutations). This evidence concerns the gene HNF4A and diabetes mellitus.