Transgenic overexpression of axonally derived NRG-1 or supplementation with soluble NRG-1 in early postnatal development was sufficient to improve the myelination status of axons and compound motor action potentials (CMAPs) on neurophysiological testing in CMT1A rodent models [195]. The gene discussed is NRG1; the disease is Charcot-Marie-Tooth disease type 1A.