In fact, as the subject’s insulin sensitivity declines, e.g. in the progression from normal to prediabetes to Type-2 Diabetes Mellitus (T2DM), the secondary insulin concentration hump is more and more pronounced, given the relative inability of the secreted insulin to force tissues to dispose of the glucose load, leading to sustained hyperglycemia and sustained pancreatic stimulation, combined with a reduced storage of the hormone in docked insulin granules. The gene discussed is INS; the disease is Hyperglycemia.