When the endothelium is injured, it stimulates the expression of inflammatory mediators, including vascular cell adhesion molecule-1 (VCAM-1), intercellular adhesion molecule-1 (ICAM-1), interleukin 6 (IL-6), and tumor necrosis factor α (TNF-α), which activate oxidative stress and the inflammatory response and induce vascular smooth muscle cell proliferation and foam cell formation, leading to plaque formation and eventually atherosclerotic lesions [9, 10]. This evidence concerns the gene ICAM1 and Atherosclerotic lesion.