With the discovery of AQP4-IgG [1, 58–60], MOG-IgG [17], N-methyl-D-aspartate receptor-IgG [61], and a plethora of often non-paraneoplastic autoantibodies identified in acute CNS inflammation over the past decade [62–66], 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 [67]. The gene discussed is MOG; the disease is myeloid sarcoma.