SCN8A and Charcot-Marie-Tooth disease type 1B: Finally, the observation that deletion of Derlin-2 causes per se a late onset demyelinating neuropathy (see below) and that its deletion synergizes with the P0-S63del mutation worsening the CMT1B phenotype, may suggest that also ERAD genes, alongside integral nodal component such as Nrcam and Scn8a [41,42,43], could be among those genetic modifiers that influence the large phenotypic variability of many forms of CMTs.