Recent studies showed the involvement of TRPM2 in pathogenesis factors of ischemic stroke as follows: by reducing oxidative stress in cardiomyocytes, TRPM2 reduces inflammation and stimulates the remodeling of the atria; it models endothelial dysfunction by deregulating the influx of calcium ions, mediates the damaging effects of ROS on the endothelium and favors hypertension; induces the death of pancreatic β cells that secrete insulin, thus promoting the development of diabetes; promotes the aggregation of platelets and favors the appearance of vascular thrombus [84–86]. This evidence concerns the gene TRPM2 and hypertensive disorder.