BRD4 and another bromodomain protein, SMARCA4, independently but concurrently activate gene expression by simultaneously binding to different regulatory elements in their target genes.6 SMARCA2, a SMARCA4 paralogue, is likely to compensate for SMARCA4 loss so that, in cancers harbouring SMARCA4/A2 deficiency, a common underlying molecular lesion, BRD4 might act as the primary driver of SMARCA4/BRD4-dependent oncogenes; consequently, exposure to BETi might eliminate this network to promote cell cycle arrest or apoptosis. Here, BRD4 is linked to cancer.