To further support the role of cerebral endothelium interactions with activated leukocytes in pathogenesis of MS and the stabilizing effect of β-interferons on the endothelial barrier, Jimenez et al [21] used an in vitro model of monocyte migration through cerebral endothelial cell monolayers to demonstrate that monocytes form complexes with CD31+EMP (monocyte:CD31+EMP complexes) and that this, in turn, facilitates transendothelial migration of monocytes. This evidence concerns the gene PECAM1 and myeloid sarcoma.