Impairment of the phosphatidylinositide 3-kinases (PI3K) – protein kinase B (AKT) – eNOS – NO pathway as a manifestation of insulin resistance contributes to endothelial dysfunction, predisposing the endothelium to hyper-inflammatory and thrombotic states, while endothelin-1 expression and mitogenic effects are not affected [17]. This evidence concerns the gene AKT1 and endothelial dysfunction.