BRD4 and CDKs are core regulators of SEs and transcription condensates that serve as targets for repressing oncogene transcription.[17] For example, BRD4 inhibition by JQ1 releases the mediator complex from a subset of SEs that drives leukemogenesis gene expression in AML.[272] In mixed‐lineage leukemia (MLL), the disruptor of telomeric silencing 1‐like (DOT1L) can induce histone H3K79 methylation, which in turn facilitates histone H4 acetylation and BRD4 binding at SEs. The gene discussed is BRD4; the disease is acute myeloid leukemia.