Transgenic mice overexpressing miR-7a in β cells developed diabetes due to impaired insulin secretion and β cell dedifferentiation, while in human, its pattern of expression oscillates responding to the extent of insulin resistance: it is reduced under moderate insulin resistance conditions, contributing to improved insulin secretion; however, it raises progressively under severe diabetic conditions and can reach levels even higher than in healthy individuals (29). The gene discussed is INS; the disease is Insulin resistance.