However, with the emergence of MOGAD as a separate disease entity and considering that these models do present drawbacks in reproducing MS characteristics (mainly CD4+ mediated, no MOG-IgG present in any form of MS, etc.)(2, 12, 35, 165–168) the issues in their translation into new therapeutic modalities for MS could be viewed in a new light (169–171). This evidence concerns the gene CD4 and myeloid sarcoma.