As the endothelial dysfunction ensued, the proinflammatory cytokines may further activate the ECs, hence increasing the expression of adhesion molecules such as VCAM-1, ICAM-1, and even EC-derived MPs (EDMPs) subpopulation such as cluster differentiation 62 (CD62E) or E-selectin. The gene discussed is SELE; the disease is endothelial dysfunction.