Another significant advancement was the redefinition of antibody-mediated autoimmune nodo-paranodopathies (neurofascin-155, contactin-1, and contactin-associated protein 1 [Caspr1]),29which used to be considered variants of CIDP.30, 31These conditions represent a completely distinct clinical entity, with clinical and pathophysiological features that differ significantly from those of typical CIDP and require specific therapeutic approaches.2 The gene discussed is CNTNAP1; the disease is chronic inflammatory demyelinating polyradiculoneuropathy.