HDAC3 expression was increased in the hippocampus and cortex of diabetic mice, and the blood-brain barrier permeability of db/db mice was decreased after the inhibition of HDAC3 activity by RGFP966, suggesting that HDAC3 may play a key role in T2DM-related neuronal diseases [20]. This evidence concerns the gene HDAC3 and type 2 diabetes mellitus.