Proatherogenic risk factors lead to endothelial dysfunction and, consequently, to increased exposure to the adhesion proteins (e.g., selectin, the intercellular adhesion molecule, ICAM, and the vascular cell adhesion molecule-1 VCAM-1) that facilitate the activation of monocytes and their adhesion to the dysfunctional area [37]. This evidence concerns the gene VCAM1 and endothelial dysfunction.