While Ccr5 deficiency resulted in reduced mononuclear cell infiltration and lesion formation as well as decreased neointima formation (184–186), combined inhibition of CCL2, CX3CR1, and CCR5 resulted in as much as a 90 % reduction in atherosclerotic plaque formation in Apoe−/− mice, in spite of persistent hypercholesterolaemia (187). This evidence concerns the gene CCR5 and Hypercholesterolemia.