Promoting the acetylation of α-tubulin by the inhibition of histone deacetylase 6 (HDAC6), a major deacetylating enzyme of α-tubulin, was shown to normalize microtubule-dependent axonal transport in mouse models of Charcot-Marie-Tooth disease with HSPB1 mutations [6], and in motor neurons derived from ALS patients with familial mutations in FUS and TDP-43 [10, 14]. Here, HSPB1 is linked to Charcot-Marie-Tooth disease.