Autoantibodies targeting theastrocytic water channel aquaporin-4 (AQP4) have emerged as a highly sensitive andspecific biomarker for the differentiation of NMOSD from MS, which is a crucialissue for an appropriate therapeutic choice.5 In fact, several MS treatments, such as interferon (IFN)-β, natalizumab andfingolimod, could lead to exacerbation of the NMOSD disease course, supporting theidea that NMOSD is distinct from MS and that NMOSD is dominated by humoralmechanisms. The gene discussed is IFNB1; the disease is myeloid sarcoma.