Since an increase in HDAC6 activity seems to be implicated in the pathogenesis of CMT2F [64], caused by mutations in HSPB1, d’Ydewalle and colleagues first tried HDAC6 inhibitors in a CMT2F transgenic mouse model, and the inhibitors corrected the axonal transport defects caused by HSPB1 mutation and reversed the CMT phenotype [65]. The gene discussed is HSPB1; the disease is Charcot-Marie-Tooth disease.