Since we observed increased A2AR surface expression during hypoxia/reperfusion, which correlated with increased hippocampal neuronal damage, and pretreatment with DRB dramatically reduced A2AR surface expression and hippocampal neuronal damage during hypoxia/reperfusion, together these results suggest that CK2 inhibition could represent a novel therapeutic target for stroke therapy. This evidence concerns the gene ADORA2A and Stroke.