As mentioned earlier, the anticancer activity of BETis could not be merely explained by their influence on the transcription of cancer driver genes, such as MYC. The promising preclinical studies on the combinatorial treatment of BETis and PARPis triggering synthetic lethality in cancer cell lines of various origin imply that suppression of DNA repair efficacy could be an essential mechanism of BETis’ anticancer effect. This evidence concerns the gene MYC and cancer.