In the last decade, we and others found that the interaction(s) between SMC and monocytes/MAC produces different inflammatory molecules including MCP‐1,17 leading to monocyte/macrophage activation, the switch of SMC towards a synthetic phenotype,18, 19, 20 and a reduction of collagen I and III expression.9 The effect of HG (ie diabetes) on MAC‐SMC cross‐talk and whether this is related to accelerated plaque evolution in diabetic patients is not known. This evidence concerns the gene CCL2 and diabetes mellitus.