In early stages of atherosclerosis development, hyperlipidemia [(cholesterol, triglyceride, and low-density lipoprotein (LDL)] promotes the retention and uptake of LDL in the sub-endothelial space (Fogelstrand and Boren, 2012), which results in activation of endothelial cells and smooth muscle cells by the upregulation of adhesion molecules [intercellular adhesion molecule 1 (ICAM-1) and vascular cell adhesion protein 1 (VCAM-1)] and secretion of chemokines [MCP-1 and macrophage colony-stimulating factor (M-CSF)] in the arterial wall (Frostegard et al., 1991). This evidence concerns the gene VCAM1 and atherosclerosis.