We have reported previously that GRK2 is induced by high glucose and insulin levels in T2DM aortas and HUVEC cells, and that an increased GRK2 expression and activation inhibits Akt/eNOS signalling/NO production, leading to impaired endothelium-dependent vascular responses (endothelial dysfunction)10, 23, 24, 29, 31. This evidence concerns the gene AKT1 and endothelial dysfunction.