Vascular smooth muscle cells are traditionally known for their role in extracellular matrix production and exhibit phenotypic plasticity, including the acquisition of plaque-promoting macrophage–like features and plaque-stabilizing fibroblast–like features.49 Classical monocytes, recruited via CCR2 and CCL2 (C-C motif chemokine ligand 2), dominate the monocyte influx in atherosclerosis and differentiate into macrophages on stimulation by mediators such as M-CSF (monocyte-colony stimulating factor). This evidence concerns the gene CCL2 and atherosclerosis.