Liang et al. [58] proved that HDAC6, a kind of histone deacetylase (HDAC), downregulated the acetylation of α-tubulin, heightened motility, and restrained autophagy in podocytes dealing with AGE, which deteriorated the phenotype of DN, suggesting that HDAC6 is a prospective target for therapy in the early phase of DN. This evidence concerns the gene HDAC9 and liver dysplastic nodule.