Inhibiting Histone Deacetylase 6 (HDAC6) compensates for the transport deficit in HD by increasing tubulin acetylation, and HDAC inhibitors enhance the vesicular transport of brain-derived neurotrophic factor (BDNF) by inhibiting HDAC6, which raises acetylation at lysine 48 of a-tubulin, thereby increasing the flux of vesicles and the subsequent release of BDNF, indicating that HDAC6 inhibition and acetylation at lysine 40 of a-tubulin could be promising therapeutic targets for disorders such as HD in which intracellular transport is disrupted [74]. This evidence concerns the gene HDAC9 and Huntington disease.