The recent discovery of disease-specific antibodies, such as anti-neurofascin 155 (anti-NF155), anti-contactin-1, anti-contactin-associated protein 1 and nodal neurofascin antibodies, that are only present in 5–10% of patients [2–4], suggests the existence of small but homogeneous subgroups of CIDP patients in which specific effector mechanisms drive the disease. Here, CNTNAP1 is linked to chronic inflammatory demyelinating polyradiculoneuropathy.