Though only EAE was analyzed in this study, astrocytes and BMECs have been suspected as critical sources of CCL2 during other neuroinflammatory conditions investigating three different CNS inflammatory scenarios (human glioma, striatal injection of LPS in mice, and adenovirally injected monkeys) reporting that extravasation of lymphocytes is mediated by CCL2-expressing astrocytes independent of the inflammatory situation and species [18]. This evidence concerns the gene CCL2 and glioma.