To further verify the effect of histone methylation and HMTs/HDMs in “metabolic memory,” results from recent cell culture studies show that transient hyperglycemia can induce the increased recruitment of the identified histone methyltransferases (HMTs) SET7/9 and histone demethylase (HDMs) LSD1 to the p65 promoter in aortic endothelial cells [33, 53], which can lead to better understanding of the basis and strategies to reduce the burden of diabetic complications such as DN. This evidence concerns the gene SETD7 and liver dysplastic nodule.