Our initial studies showed that KDM3A could promote vascular neointimal hyperplasia in diabetic rats via the AGTR1 and ROCK2 signalling pathways.15 KDM3A inhibition could also attenuate high concentration insulin–induced vascular smooth muscle cell injury by suppressing MAPK/NF–κB pathways.17 In addition, our latest findings suggest that KDM3A is involved in diabetic cardiomyopathy and is a crucial factor in mediating myocardial ‘Metabolic Memory’ injury in diabetes by facilitating NF‐κB/p65 transcriptional activities. This evidence concerns the gene KDM3A and diabetes mellitus.