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. This evidence concerns the gene ADAM17 and neuropathy.