Consistent with this, knockdown of BRD4 by RNAi, or disruption of its binding to acetylated chromatin by BET inhibitors (BETi) leads to lethality in AML blast progenitor cells (BPCs), associated with down regulation of AML-relevant progrowth and prosurvival oncogenes1,2,10–13. The gene discussed is DNER; the disease is acute myeloid leukemia.