Mechanistically, we show that ectopically expressed BRDT forms an active PTEFb complex that colocalizes with active transcription in lung cancer cells; that it can compensate for BRD4 loss in the transcriptional response to hypoxic stress; and that, similar to BRD4, it can release paused Pol II independently of its bromodomains. This evidence concerns the gene BRD4 and lung carcinoma.