In order to cope with high levels of replicationstress, cancer cells depend on ATR for survival and proliferation (Choi et al., 2011; Toledo et al., 2011a).Therefore, pharmacological inhibition of ATR selectively sensitizes different typesof tumor cells, especially in tumors with defects in the ATM-p53 pathway (Charrier et al., 2011; Peasland et al., 2011; Reaper et al., 2011; Toledo et al., 2011b; Fokas et al., 2012; Foote et al., 2013, 2015, 2018; Kim et al.,2018). This evidence concerns the gene ATR and cancer.