Hyperglycemia can contribute to oxidative stress through the production of mitochondrial superoxide, NADPH reduction through polyol accumulation, and AGE synthesis through the nonenzymatic oxidation of glycoproteins—all of which are capable to cause damage to the endothelial cells; the vascular endothelium is particularly sensitive to the effects of hyperglycemia since endothelial cells do not adaptively downregulate their GLUT-mediated uptake of glucose [34–37]. The gene discussed is SLC2A1; the disease is Hyperglycemia.