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). The gene discussed is DAPK1; the disease is cerebral artery occlusion.