In addition, it was shown that microtubule protein acetylation deficiency decreases in vitro molecular motor kinesin-1 binding and transport, while increased microtubule protein acetylation mediated by inhibition of HDAC leads to recruitment of kinesin and kinesin-1 into microtubules, thereby compensating for the intracellular transport defect in Huntington’s disease [94]. The gene discussed is KIF5C; the disease is Huntington disease.