Emerging evidence suggests that ox-LDL exposure is associated with upregulation of ICAM-1 and VCAM-1, as well as inactivation of the PI3K-Akt-eNOS signaling cascade in multiple cell types; however, the mechanism by which adhesion molecules and Akt/eNOS are regulated in ox-LDL-induced endothelial dysfunction has not been fully elucidated [31–33]. Here, AKT1 is linked to endothelial dysfunction.