In addition, the disturbance of the pancreatic microcirculation in AP leads to the lack of adequate supply of glycogen in local pancreatic tissues, which accelerates the depletion of glycogen in acinar cells and eventually induces the depletion of ATP as the result of an increased anaerobic glycolysis capacity associated with “no glucose for glycolysis.” Therefore, it is not the best compensatory mechanism to regulate energy metabolism through enhancing glycolysis of the acinar cells by activated HIF-1α. The gene discussed is HIF1A; the disease is alkaline phosphatase measurement.