LRRK2 and Parkinson disease: Increases in MT acetylation caused by the α-tubulin acetyltransferase αTAT1 or deacetylase inhibitors prevent the interaction between LRRK2 mutants and MTs, and genetic inhibition of HDAC6 or SIRT2 or administration of the SIRT2 inhibitor AGK2 reverses the defective axonal transport and locomotor behavior induced by LRRK2 mutants [27], indicating that deacetylase inhibitors targeting HDAC6 or SIRT2 are potential therapeutics for axonal transport dysfunction in mutant LRRK2-related PD.