Damage to these cells begins when fasting blood glucose levels are still normal but there are already extensive post-prandial hyperglycaemic peaks 37, leading to the proposal that the crucial mechanism for vascular damage is insulin resistance, which is characterized by a close connection between hyperglycemia, increased dense and small LDL, vascular endothelial dysfunction, morphological alterations of the vascular wall and coagulation. The gene discussed is INS; the disease is Hyperglycemia.