In summary, the present study shows TRPM2 activation during reperfusion as a crucial mechanism responsible for the delayed increases in the [Zn2+]c that drives transient ischemia-induced CA1 pyramidal neuronal death and memory impairments, and suggests that TRPM2 inhibition is a promising strategy of developing novel therapeutic treatments to mitigate the cognitive sequelae following transient ischemia or stroke. The gene discussed is TRPM2; the disease is memory impairment.