As phosphorylation of Tie2 triggered by Ang1 binding has been reported to activate specific intracellular signal molecules, including FAK, Akt, and mitogen-activated protein kinase (MAPK) (ERK1/2), in endothelial cells12,14, it seems that α5β1 integrin interaction with Ang1/Tie2 enhanced the activation of Tie2 and its downstream effectors FAK and Akt in BECs after cerebral ischemia. This evidence concerns the gene MAPK3 and brain ischemia.