In LDL receptor (LDLR)‐deficient mice (a hypercholesterolaemic model that spontaneously develops atherosclerosis when fed on a fat‐rich diet), knockout of CXCR2 resulted in attenuated atherogenesis indicating the pro‐atherosclerotic role of increased expression of this receptor, especially in neutrophils 24. Here, LDLR is linked to atherosclerosis.