In a physiological setting, the earliest mechanisms regulating postprandial hyperglycemia involve: (i) the readily releasable pool of insulin granules; (ii) the membrane translocation of glucose transporters in insulin-target tissues; (iii) post-translational regulatory mechanisms, mostly based upon post-translational modifications (i.e., phosphorylation), which affect enzyme functions that are implicated in carbohydrate metabolism, glucose homeostasis and disposal. The gene discussed is INS; the disease is Hyperglycemia.