Utilizing the TRPM2-derived interfering peptide TAT-EE3, the authors demonstrated that disruption of the TRPM2-NMDAR interaction effectively prevented phosphorylated CREB and ERK1/2 levels, inhibited neuronal excitotoxicity, and protected mice from ischemic stroke in vitro and in vivo (Zong et al., 2022b). This evidence concerns the gene TRPM2 and ischemic stroke.