In this setting, phosphorylation of GCN5 at Ser275 was also inhibited (Fig. 9d), indicating that disruption of the GCN5-CITED2-PKA signalling module by CITED2 depletion attenuates gluconeogenesis and ameliorates hyperglycemia through suppression of GCN5 phosphorylation at Ser275 and consequent enhanced GCN5-dependent acetylation and inhibition of PGC-1α as well as reduced GCN5-dependent acetylation of histone H3K9. The gene discussed is KAT2B; the disease is Hyperglycemia.