Intracellular adhesion molecule (ICAM), vascular cell adhesion molecules (VCAM), and monocyte chemoattractant protein-1 (MCP-1) promotes the infiltration of monocytes to the vascular wall and leads to an increase in local, causing endothelial dysfunction consequently—a key point of atherosclerotic plaque genesis [5,6]. This evidence concerns the gene CCL2 and endothelial dysfunction.