Importantly, binding selectivity of msR4M-L1 for MIF versus CXCL12 was functionally paralleled in a number of inflammation- and atherosclerosis-relevant cell systems, i.e. GPCR/CXCR4 signaling, 2D lymphocyte chemotaxis, foam cell formation, monocyte adhesion under static and flow conditions, and 3D monocyte migration, together representing MIF/CXCR4-mediated cell systems with disease relevance41. Here, MIF is linked to atherosclerosis.