If the genomic distribution of PARP1‒BRG1‒EP300 complexes is similar in proliferating cancer cells and macrophages, then interference with PARP1 displacement may impact the intracellular processes listed in the abovementioned paper by Sobczak et al. Again, the molecular switch that makes the transcription machinery dependent on PARP1 physical interaction with chromatin or poly-ADP-ribosylation of co-operating enzymes BRG1 and EP300 remains unknown. This evidence concerns the gene EP300 and cancer.