Even if a higher proportion of low-titer MOG-IgG in MS compared to other diseases was systematically demonstrated, an additional challenge would be discerning whether low levels of MOG-IgG in this context contribute to immunopathogenesis or are an epiphenomenon of MS-related demyelination, i.e., whether the antibody is of clinical relevance or not; this adds a layer of complexity to both diagnostic accuracy studies and clinical practice that would benefit from dedicated evaluation. This evidence concerns the gene MOG and myeloid sarcoma.