This “crossover effect” of KATP current density on insulin secretion likely contributes to the progressive decline in β cell function that occurs as people progress from obesity and normal glycemic control (insulin hypersecretion) to obesity and prediabetes (insufficient insulin secretion) or to obesity and T2D (markedly impaired insulin secretion) (2, 27, 28). This evidence concerns the gene INS and type 2 diabetes mellitus.