However, the studies in an animal model of MS (experimental autoimmune encephalomyelitis, EAE) have revealed that CHI3L1 might also promote oligodendrogenesis (the process of generating new oligodendrocytes) by the activation of the epidermal growth factor receptor (EGFR) and the mitogen-activated protein kinase (MAPK) signaling pathway [147]. This evidence concerns the gene EGFR and experimental autoimmune encephalomyelitis.