Hard evidence shows that inflammatory hyperactivity, together with increased expressions of adhesion molecules such as vascular cell adhesion molecule-1 (VCAM-1), intercellular adhesion molecules (ICAMs) and CD62 antigen-like family member E (E-selectin) on vascular endothelial cells are the hallmarks of early atherosclerosis by recruiting inflammatory cells to the vessel wall facilitating their transendothelial migration [15]. The gene discussed is SELE; the disease is atherosclerosis.