Our recent study indicated that A2KO mice displayed blood–brain barrier (BBB) dysfunction, and exogenous administration of recombinant AnxA2 (rA2) protected against hypoxia plus IL-1β-induced cerebral trans-endothelial permeability [16], implying that AnxA2 might be a key endogenous factor that functions in reducing pro-inflammatory response after acute brain injury. This evidence concerns the gene ANXA2 and injury.