In short, the combination of DAPK1-NR2B receptor subunit mediates pathological process of stroke injury, including necrosis, apoptosis and autophagy of neuronal cells (Figure 2), and most importantly, it is not relevant to physiological function of NMDA receptor because the interrupting of DAPK1 with NR2B does not alter the synaptic transmission of NMDA receptor [39]. This evidence concerns the gene GRIN2B and Stroke.