Treatment with TRPM2 inhibitors, TRPM2-shRNA, or genetic ablation of TRPM2 expression did not significantly diminish delayed neuronal death in female mice following cardiac arrest-resuscitation (CA-R), reduce cerebral infarction in female mice subjected to middle cerebral artery occlusion-reperfusion (MCAO-R), or decrease delayed neuronal death in female mouse cortical and hippocampal neurons induced by OGD/R in vitro (139–141). The gene discussed is TRPM2; the disease is cardiac arrest.