HDAC4 is regarded as a contributor to podocyte injury in type 1 and type 2 diabetic models and diabetic patients and could suppress autophagy related with podocyte injury in DN by deacetylating STAT1, suggesting that HDAC4 is important to accelerate DN in epigenetic and nonepigenetic mechanisms [70, 71]. Here, STAT1 is linked to liver dysplastic nodule.