In a demyelination model used in the study of MOG-35-55-induced experimental autoimmune encephalomyelitis (EAE) [29,30], the crucial role of IL-6 in the induction phase of EAE was reported by Y. Okuda et al. [29], and the protective effect of IL-6 blockade against EAE via the inhibition of Th17 cells’ development was reported by Satoshi Serada et al. [30]; the results suggested that IL-6 may be involved in demyelination. The gene discussed is MOG; the disease is experimental autoimmune encephalomyelitis.