Moreover, in our recent study, we found that TRPM2 was able to physically and functionally associate with GluN2a and GluN2b in NMDAR at extrasynaptic sites, and specific disruption of this TRPM2-NMDAR interaction using a interfering peptide produced a protective effect against ischemic stroke similar to Trpm2 deletion [57]. The gene discussed is GRIN2A; the disease is ischemic stroke.