In summary, we conclude that glial NRG1 functions as a key driver of histopathological hallmarks including hypermyelination and onion bulb formations in CMT1A disease, which prompted us to test whether chronically increased Schwann cell-derived NRG1 signaling is sufficient to induce aspects of CMT1A pathology in vivo. This evidence concerns the gene NRG1 and Charcot-Marie-Tooth disease type 1A.