CNTNAP1 and chronic inflammatory demyelinating polyradiculoneuropathy: It is worth noting that the pathogenic mechanism of IgG4 antibodies in other diseases implicates the disruption of cell adhesion protein complexes too, by inhibiting protein-protein interaction, and that therapies aiming at downregulating the humoral immune response, such as rituximab, showed some efficacy in anti-Nfasc155- and anti-Caspr1 antibody-associated CIDP, as well as in other IgG4-related diseases, likely because of the depletion of the Nfasc155- or Caspr1-reactive B cells.26