NMNAT2 and Wilson disease: WD was first described in frogs by the British physician Augustus Waller in the mid-19th century,1 and it has been observed in a diverse group of animal models2 including Drosophila,3,4 zebrafish,5,6 and mouse.7 WD follows a morphological sequence that consists of a latent phase, followed by beading, thinning, fragmentation, and finally clearance of axonal debris.8 More recently, the molecular mechanisms that execute WD have been elucidated, where upon injury, the transport of the short-lived NAD-synthase NMNAT2 to axons is disturbed.