The two-in-one protein structure, ubiquitous distribution throughout the body, and redox-sensitive Ca2+-permeable cation channel enabled the involvement of TRPM2 in numerous pathophysiological processes, such as oxidative stress, apoptosis and necrosis, pulmonary inflammation, Alzheimer’s disease, ischemic stroke, hypoxic-ischemic brain damage, neurovascular injury, renal inflammation and fibrosis, pancreatitis, liver damage, ischemia–reperfusion injury (IRI), diabetes mellitus, and tumorigenesis [12, 15, 17–44]. Here, TRPM2 is linked to ischemic stroke.