Shen et al. recently demonstrated that ATR and ARID1A directly interact and loss of this interaction in HCT116 ARID1A−/− tumour cells results in impaired ATR activation (as measured by ATR autophoshorylation) in response to ionizing radiation, although ATR signalling in response to agents that stall replication forks such as hydroxyurea (HU) and ultraviolet radiation appeared normal32. This evidence concerns the gene ATR and neoplasm.