Disrupting the protein–protein interactions between BRD4 and acetyl-lysine can effectively repress the transcription of c-Myc oncogene and c-Myc dependent genes and inhibit the proliferation of cancer cells such as AML, the activated B-cell-like subtype (ABC) of diffuse large B-cell lymphoma (DLBCL)35–37, neuro-blastoma38 and lung adenocarcinoma.39 Here, BRD4 is linked to lung adenocarcinoma.