This hypothesis was confirmed by our data, which we obtained by immunizing control monocyte-derived M1-Mφ and M2-Mφ with the highly encephalitogenic peptide myelin oligodendrocyte glycoprotein (MOG35-55), by which M1 and M2 phenotypes partially mimicked those obtained from EAE-induced macrophages, possibly indicating that the changes in macrophage function could play an important role in the pathogenic mechanisms triggered by this peptide upon the induction of encephalomyelitis. This evidence concerns the gene OMG and encephalomyelitis.