With the discovery of AQP4-IgG [1, 6, 48], MOG-IgG [10], N-methyl-D-aspartate receptor-IgG [49], and a plethora of often non-paraneoplastic autoantibodies identified in acute CNS inflammation over the past decade [50–54], including in patients with primary or secondary demyelination, it becomes increasingly clear that not all patients presenting with relapsing CNS disease of putative autoimmune etiology have classical MS – even if they formally meet the ‘positive’ clinicoradiological criteria for MS [46]. This evidence concerns the gene MOG and myeloid sarcoma.