Chemokines recruit blood cells to sites of inflammation, where they adhere to and transmigrate through the vascular endothelium. Sustained high chemokine expression eventually leads to plaque formation. We have identified MIF as an atypical chemokine and noncognate CXC chemokine receptor ligand involved in atherosclerosis, acting through interaction the chemokine receptors CXCR2 and CXCR4 (ref. 1). Applying an in vitro adhesion assay, we have demonstrated that MIF induces monocyte arrest under shear stress.