Our preclinical studies confirmed that treatment with the ATR inhibitor ceralasertib (AZD6738) induces selective cytotoxicity and chemosensitization of TP53- or ATM-defective CLL cells, as well as in CLL patient-derived xenograft models with biallelic TP53 or ATM loss, in which treatment with ceralasertib led to a reduction not only in tumor load, but also in the proportion of CLL cells with these genetic defects [68]. The gene discussed is ATR; the disease is neoplasm.