DAPK1 was recruited to the NR2B protein complex after transient middle cerebral artery occlusion (tMCAO), binding to a unique region of the NR2B C-terminal region, phosphorylating NR2B and upregulating channel current; administration of a peptide uncoupling DAPK1 from NR2B or genetic deletion of DAPK1 reduced infarction after tMCAO and selective neuronal death after TGI (Tu et al., 2010). This evidence concerns the gene GRIN2B and cerebral artery occlusion.