CA2 and ischemic stroke: As a Ca2+‐permeable channel, previous studies show that TRPM2 channel is involved in excitotoxicity in ischemic stroke via coupling with synaptic NMDARs and increased endogenous bilirubin can activate TRPM2 channel to aggravate Ca2+‐dependent brain injury in stoke patients and mouse models [27, 59], suggesting TRPM2 channel can regulate the excitatory of neurons.