In DLBCL, several key oncogenic pathways, including those driven by MYC- or E2F-dependent transcription and proliferation or Toll-like receptor signalling, are transcriptionally regulated by BET proteins.15 In preclinical models, BET inhibition impedes BRD binding to super-enhancer sites for MYC and other important transcription factors,15,19,20 thereby disrupting key lineage-specific transcriptional programs and resulting in anti-lymphoma activity. This evidence concerns the gene DNER and diffuse large B-cell lymphoma.