In an effort to elucidate the mechanism of KC/CXCR2 in atherosclerosis, Boisvert et al. utilized LDLR–/–, atherosclerosis-prone mice with KC/GRO-α–/– and CXCR2–/– mice to demonstrate that overexpression of KC/GRO-α and CXCR2 are essential to macrophage accumulation into atherosclerotic lesions. This evidence concerns the gene CXCR2 and atherosclerosis.