This is perhaps unsurprising in view of the importance of Schwann cell axonal interaction in neuronal maintenance and previous observations that the degree of disability in demyelinating CMT1A is due to the degree of axonal loss rather than the degree of conduction velocity slowing (a surrogate marker of demyelination).24 This finding also suggests that plasma NfL concentration may show promise as a biomarker of disease activity in other demyelinating peripheral neuropathies such as Guillain-Barré syndrome and chronic inflammatory demyelinating polyneuropathy. This evidence concerns the gene NEFL and Charcot-Marie-Tooth disease type 1A.