Unfortunately, MOGAD’s clinical course and variant phenotypes are not well elucidated in the literature in contrast to MS and NMOSD, and its clinical and radiological similarities to other demyelinating disorders often lead to misdiagnosis. So far, the most common way to diagnose MOGAD is with the presence of serum MOG-IgG1 antibodies in conjunction with radiologic-positive demyelinating lesions and clinical findings. Here, MOG is linked to demyelinating disease.