Furthermore, IS was involved in the pathophysiology of atherosclerosis by increasing the expression of the adhesion molecules intercellular adhesion molecule-1, vascular cell adhesion molecule-1, monocyte chemotactic protein-1, and e-selectin [62,63], and activating the p42/44 mitogen-activated protein kinase (MAPK) pathway and thus vascular smooth muscle cell (VSMC) proliferation [64]. This evidence concerns the gene CCL2 and atherosclerosis.