Treatment with excess SeP inhibited VEGF-stimulated proliferation and the phosphorylation of VEGFR2 and ERK2 in HUVECs, which was significantly improved by the addition of buthionine sulphoximine (BSO), an inhibitor of glutathione synthesis.(76) Therefore, the adverse effects of increased SeP in type 2 diabetes are diverse and might be related to vascular complications. Here, KDR is linked to type 2 diabetes mellitus.