Liraglutide improves EPC dysfunction under diabetic conditions predominantly through increasing Nrf2 activation via the AKT/GSK-3β/Fyn pathway, and subsequently increases antioxidative genes expression, ameliorates oxidative stress and restores the bioavailability of NO, therefore protecting EPC from diabetes and HG-induced dysfunction, and promoting ischemic angiogenesis under diabetic conditions, as illustrated in Figure 8J. This evidence concerns the gene GSK3B and diabetes mellitus.