Deregulation of insulin signaling leads to altered endothelial phosphatidylinositol 3-kinase (PI3K)/protein kinase B (Akt) pathway; therefore, endothelial cells lessen NO synthesis, so that decreased vasodilatation and increased blood pressure occur; moreover, activation of the renin-angiotensin system increases expression of mineral corticoid receptors in kidney, with subsequent sodium re-absorption and hypertension [96]. Here, AKT1 is linked to hypertensive disorder.