Our previous study indicated that SETD8 is involved in many pathways associated with hyperglycemia-mediated endothelial injury, such as high-glucose-induced endothelial proinflammatory enzyme and proinflammatory cytokine production, NOD-like receptor pyrin domain 3 inflammasome (NLRP3)activation, antioxidant imbalance, and endothelial adhesion molecule expression [25–27]. This evidence concerns the gene KMT5A and Hyperglycemia.