The mechanism of SET8 regulation in human umbilical vein endothelial cells (HUVECs) with hyperglycemia showed that low expression of SET8 increased the production of cellular ROS, leading to increased oxidative stress, while overexpression of SET8 attenuated oxidative stress damage to endothelial tissue by blocking ROS accumulation [27]. This evidence concerns the gene KMT5A and Hyperglycemia.