Cells repair the breaks, but repair is imperfect, and repeated rounds of breaking and mending seed the mutations that let tumors evolve. They combined those maps with markers of transcription stress, including gamma H2AX, a protein signal cells deploy at sites of DNA damage. Hidmi added that because cancer cells depend on these high-stress regions to keep growing, they may also be more vulnerable there. Cancer cells repair most of this damage successfully. Drugs that interfere with runaway transcription or with DNA repair are the implied direction, but nothing has been tested.