Indeed, we also found that oxygen–glucose deprivation (OGD), an in vitro mimic of ischemic stroke, induced substantial ROS production and hyperpermeability in CECs, whereas Trpm2 deletion or TRPM2 inhibition protected CECs from OGD-induced Ca2+ overload, tight-junction degradation, and endothelial hyperpermeability (under revision). The gene discussed is TRPM2; the disease is ischemic stroke.