Our results led to a working model that BRD4 regulates MYC through a transcription-independent mechanism by means of the BRD4-NSD3-MYC pathway, in addition to the well-established BRD4-pTEFb-mediated pathway (Fig. 4k), which may have significant clinical implications for the response of MYC-driven tumours to BRD4 inhibitors that are currently in clinical trials. This evidence concerns the gene BRD4 and neoplasm.