Experimental evidence so far supports the notion that the anti-proliferative effects observed in MLL-fusion driven leukemia upon inhibition of BRD4 was, at least in part, due to the downmodulation of MYC, BCL2 and CDK6 [8,19] but it has remained unclear whether BRD4 is directly recruiting the MLL-AF9 protein to chromatin or whether BRD4 inhibition would act on independent molecular pathways. The gene discussed is BCL2; the disease is leukemia.