The interaction and regulation of GluN2B-containing NMDAR by death-associated protein kinase 1 (DAPK1) has attracted the interest of the investigators in the field of stroke since a peptide that prevents the interaction of the kinase with GluN2B protected brain damage induced by middle cerebral artery occlusion (MCAO), a model of focal brain ischemia, without affecting the physiological activation of NMDAR [85, 86]. This evidence concerns the gene GRIN2B and stroke disorder.