Previous studies have demonstrated that hyperglycemia causes endothelial dysfunction by four major mechanisms: (i) increased glucose flux into the polyol pathway; (ii) increased intracellular production of advanced glycation end-products (AGEs); (iii) activation of protein kinase C (PKC) isoforms; (iv) overactivity of the hexosamine pathway [see review (57)]. The gene discussed is PRRT2; the disease is Hyperglycemia.