In a mouse model of T2DM, HDAC3 inhibition by its specific inhibitor RGFP966 upregulated miR-200a, thereby reducing the Keap1–Nrf2 interaction and promoting Nrf2 activation, which in turn significantly ameliorated the BBB permeability and TJ protein downregulation associated with T2DM [114]. This evidence concerns the gene KEAP1 and type 2 diabetes mellitus.