This interaction causes stabilisation of the stalled forks, suppression of further replication origin firing and cell cycle arrest (intra-S and G2/M phases).13 Hypomorphic mutations in human ATR cause the rare autosomal-recessive disease Seckel syndrome, and complete loss of ATR in mice leads to embryonic lethality, although partial suppression is compatible with life.14 However, small molecule inhibition of ATR in cell lines results in enhanced sensitivity to radiation, although to a lesser extent than ATM inhibition.15,16. This evidence concerns the gene ATR and Seckel syndrome.