Depletion of GCN5 or expression of the phosphorylation-defective mutant GCN5(S275A) in the liver of mice with obesity and type 2 diabetes suppressed gluconeogenesis and thereby improved glycemia, suggesting that inhibition of GCN5 expression or phosphorylation at Ser275 may ameliorate diabetes. This evidence concerns the gene KAT2B and type 2 diabetes mellitus.