Since we previously reported [20] that A1Rs are downregulated while A2ARs are upregulated after focal cortical ischemia, and previous reports by others demonstrating that CK2 negatively regulates A2AR desensitization rate [140], it is therefore plausible to suggest that the observed downregulation of CK2 in our focal cortical ischemic stroke model could be mediated in part by the prolonged A1R activation and subsequent A1R desensitization after stroke. This evidence concerns the gene ADORA2A and stroke disorder.