Considering the gain-of-function mutations of α-syn and LRKK2 in PD and the contribution of deacetylated α-tubulin to their neurotoxicity, as well as the role of HDAC6 in protein aggregate degradation and autophagy [116], targeting SIRT2 inhibition may be a valuable potential therapeutic strategy for α-syn- or LRKK2-related PD. This evidence concerns the gene HDAC6 and Parkinson disease.