Some other studies showed that H3K4me3 at proinflammatory genes (MCP-1 and TNF-α), profibrotic genes (TGF-β1 and collagen III), and histone-modifying enzyme (Set1 and BRG1) were increased in renal ischemia-reperfusion injury animal models [58, 59], which provide hints for the DN underlying mechanism study in the future. This evidence concerns the gene CCL2 and liver dysplastic nodule.