It is well established that Cx32/GJB1‐null mice (CMT1X model) exhibit CMT‐like neuropathy with slowed conduction and progressive myelin defects (Nelles et al. 1996; Anzini et al. 1997), whereas MAG‐null mice (Montag et al. 1994; Weiss et al. 2001) display related myelin and functional abnormalities and have been suggested to mimic aspects of HNPP (Yin et al. 1998). The gene discussed is MAG; the disease is neuropathy.