This is clearly in contrast to our recently published data about longitudinal GCIP thinning in AQP4-IgG-seropositive NMOSD [22] or earlier studies reporting GCIP loss in MS [27] and might be an important hint towards the differentiation of MOG-IgG-associated diseases from AQP4-IgG-seropositive NMOSD. This evidence concerns the gene AQP4 and myeloid sarcoma.