The importance of GCN5-MYC interactions is highlighted by the finding that deletion of GCN5 in the Eμ−MYC mouse model of B-cell lymphoma significantly extends mouse survival in concert with destabilization of MYC protein and downregulation of MYC target genes that normally promote proliferation of B cell precursors over differentiation (81). The gene discussed is KAT2A; the disease is B-cell non-Hodgkin lymphoma.