Sir, The concept of nodo-paranodopathy was first applied to axonal Guillain-Barré syndrome subtypes with antibodies to gangliosides, then extended to some patients classified as chronic inflammatory demyelinating polyradiculoneuropathy (CIDP) carrying IgG4 antibodies against paranodal axo-glial proteins, to focus on the site of nerve injury, to reminding specific pathophysiological mechanisms and reconcile contrasting electrophysiological and pathological findings (Uncini et al., 2013; Uncini and Vallat, 2017). In 2017, in an article published in Brain by Delmont et al., the authors observed that anti-Nfasc (neurofascin) 140/186 IgG3 are associated with a subset of CIDP patients. They suspected that these antibodies induce functional alterations at nodes, without any pathological study (Delmont et al., 2017). We herein report the first electrophysiological and pathological description of a patient with nodopathy and anti-Nfasc140/186 IgG3 antibodies. A male, in his 70’s, was admitted because of numbness of hands followed by weakness in the four limbs, which began 8 days before. No previous infection was detected. Examination showed predominantly proximal motor weakness of the four limbs, generalized areflexia, distal loss of pinprick and vibration sense at the four limbs, and mild respiratory failure. Serology for HIV, hepatitis B and C viruses, cytomegalovirus, Epstein-Barr virus, Campylobacter jejuni and Borrelia burgdorferi was negative. No antibodies to glycolipids were detected. Spine MRI, CSF, VEGF and serum complement (C3-C4-CH50) were normal. Serum immunofixation revealed IgA-lambda monoclonal gammopathy and bone marrow aspiration a low-grade IgA-lambda myeloma. No bone lesions were found on the whole-body radiography. Intravenous immunoglobulin (IVIg) was given (0.4 g/kg/day  5 days) and the patient improved, such that he could walk again. Almost 3 weeks after the end