Conversely, increased fibrotic and ECM levels induced by hyperglycemia and changes in promoter H3Kac and H3Kme, as well as SET7 recruitment, were significantly blocked by TGF-β1 antibody treatment, emphasizing the significant role of TGF-β1 in hyperglycemia-induced epigenetic histone modifications [62, 63]. The gene discussed is SETD7; the disease is Hyperglycemia.