A hallmark of the early stages of T2D is insulin resistance, i.e. an impaired insulin-mediated cellular uptake of glucose, while advanced stages are characterized by a dysfunction of pancreatic β-cells, leading to insufficient insulin secretion and overt hyperglycemia.[3–6] Defined animal models that mirror the pathogenesis in humans have played a valuable role in studying the complex manifestation of T2D and for assessing new treatment modalities. The gene discussed is INS; the disease is Hyperglycemia.