In particular, montelukast reduced ox-LDL-induced adhesion of monocytes to endothelial cells, suppressing VCAM-1 and E-selectin expression6, delayed the progression of atherosclerosis and intimal hyperplasia7 by inhibiting the expression of monocyte chemoattractant protein 1 (MCP-1)8 and matrix metalloproteinases (MMPs)9, and prevented aortic dilatation, rupture and aneurism development10. The gene discussed is CCL2; the disease is atherosclerosis.