We have recently found that CDM inhibits EBV replication through overgeneration of ROS (reactive oxygen species) in EBV-associated tumors (20), and that it also increases p300 over-acetylation in acute myeloid leukemia (AML) cells with dissociation of p300 from HIF1α, subsequently suppressing the HIF1α/VEGF pathway (21). The gene discussed is VEGFA; the disease is acute myeloid leukemia.