Our findings are in line with molecular and pathophysiological consequences of insulin resistance in endothelial cells [1,2,6]: While in metabolically healthy individuals insulin acts as a vasoactive hormone, primarily by activating phosphatidylinositol 3-kinase (PI3K) and consequently nitric oxide production (due to Akt mediated phosphorylation of endothelial nitiric oxide synthase), this signaling pathway is notably blunted by insulin resistance leading to impaired endothelium dependent vasodilatation. The gene discussed is INS; the disease is Insulin resistance.