Extracellular accumulation of EAAs during ischemic stroke can excite NMDAR1 and resultant Ca2+ influx, which further destroy the mitochondrial membrane potential, leading to the damage of mitochondrial, decreases in ATP synthesis, dysfunction of Na+/K+-ATPase, and finally cell apoptosis in ischemic neurons [25, 26]. This evidence concerns the gene GRIN1 and ischemic stroke.