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. The gene discussed is KAT2A; the disease is obesity due to melanocortin 4 receptor deficiency.