The chemokine CCL2, which is elevated during CNS inflammation and is associated with endothelial dysfunction, transiently induces Src-dependent disruption of hCMEC/D3 AJs, translocation of β-catenin from the AJ to PECAM-1, and increases surface localization of PECAM-1[14]. The gene discussed is PECAM1; the disease is endothelial dysfunction.