The histone deacetylase HDAC3 was also activated in the thoracic aortic endothelium of db/db mice, and its inhibition prevented high glucose- and palmitic acid-induced dysfunction in HUVECs by decreasing Keap1 synthesis to increase Nrf2 levels and downregulate Nox4, which suggests that HDAC3 is a target for the treatment of endothelial dysfunction in T2DM [102]. The gene discussed is NOX4; the disease is endothelial dysfunction.