Based on these observations one would infer from other cancer entities that there might be therapeutic synergism with other agents that put additional stress on DNA repair pathways, and in fact the authors found ATM-deficient tumor cells to be twofold more sensitive to EF24 treatment than matched wild-type controls; moreover, it was observed that EF24 specifically sensitized FA-competent cells to mitomycin C, a DNA crosslinker previously described to be particularly active in cancer cells with defective DNA repair pathways, including molecularly defined subsets of pancreatic cancer [39]. The gene discussed is ATM; the disease is cancer.