Furthermore, studies using Trpm2 gene knockout (KO) mice have revealed that H2O2-activated Ca2+ influx through TRPM2 contributes to innate immune responses via chemokine production in monocytes [119], neutrophil adhesion during myocardial ischemia/reperfusion injury [39], and NLRP3 inflammasome activation in macrophages [122]. Here, TRPM2 is linked to myocardial ischemia.