Consistent with this observation, like in HCT116 p53 null and p53R273H, we also found a 5- to 10-fold enhanced etoposide sensitivity when ATR is pharmacologically inhibited in other cancer cell lines deficient in p53 (SaOS2 and H1299) or endogenously expressing the p53R273H mutant (MDA-MB-468) (Supplementary Figure 6C). Here, TP53 is linked to cancer.