ATF4 and Charcot-Marie-Tooth disease type 1B: 2002; van der Voorn et al. 2005). Similarly, mouse models of Pelizaeus–Merzbacher, vanishing white matter diseases and Charcot–Marie–Tooth (CMT1B) peripheral neuropathy mouse models all display expression of UPR markers such as CHOP, ATF4 and XBP1s (van Kollenburg et al. 2006; Pennuto et al. 2008; Southwood et al. 2013). In CMT1B, UPR modulation is therapeutic (D'Antonio et al. 2013; Das et al. 2015). Mouse models of the dysmyelinopathy, X‐linked adrenoleukodystrophy, similarly show UPR overactivation (Launay et al. 2017).