ADAM17 and hereditary neuropathy with liability to pressure palsies: Here, we provide evidence that Niaspan—by modulating Tace activity and, hence, PNS myelination—represents a valid approach for the treatment of CMT4B1 and HNPP neuropathies, which may be extended to other forms of CMT characterized by excessive myelin such as CMT4B2, B3, and CMT4H.