In the current review, we discuss the functional and structural phenotypes related to ON in currently used mouse models, and summarize how the pathophysiology and visual phenotype of the myelin oligodendrocyte glycoprotein 35-55 (MOG<sub>35 - 55</sub>) experimental autoimmune encephalomyelitis (EAE) mouse model recapitulates clinical features of multiple sclerosis (MS), myelin oligodendrocyte glycoprotein antibody-associated disease (MOGAD), and neuromyelitis optica spectrum disorder (NMOSD). This evidence concerns the gene OMG and experimental autoimmune encephalomyelitis.