VE-821 selectivity is based on the concept that (i) more than 50% of cancer cells have lost their G1-phase checkpoint for example due to p53 mutation/deletion and thus rely on S- and G2-checkpoints; which are known to be regulated by ATR and (ii) cancer cells with activated oncogenes generate replication stress at much higher levels than normal cells, thus activating ATR [8,9]. This evidence concerns the gene ATR and cancer.