The proliferation of vascular smooth muscle cells (VSMCs) is a key step of atherosclerosis.2 One mediator in formation of lesion in humans may be focal build‐up of intimal VSMCs.3 However, there is still debate in the accurate role of VSMCs in atherosclerosis.4 In early stage of atherosclerosis, VSMCs may be a contributor to the formation of the atheroma through the synthesis of matrix molecules necessary for the retention of lipoproteins and through the generation of pro‐inflammatory mediators including vascular cell adhesion molecule and monocyte chemoattractant protein 1.3 The gene discussed is CCL2; the disease is atherosclerosis.