LIF and CNTF play a protective role in oligodendrocyte survival in vitro [48] and in vivo [49]; furthermore, in an experimental autoimmune encephalomyelitis (EAE) animal model of multiple sclerosis (MS), double deletion of LIF-R and gp130 to inhibit STAT3 activation worsened MS-induced demyelination when compared to wild-type animals [50]. The gene discussed is CNTF; the disease is experimental autoimmune encephalomyelitis.