We show this at clinically relevant concentrations and doses of ATRi, WEE1i and CHK1i where their single-agent activity shows no differential effects in SLFN11-proficient versus SLFN11-deficient cancers, as well as at clinically relevant concentrations of DDA.38–41,47 We also demonstrate, the combinations restore/induce DNA damage and replication stress and ultimately induce cell death in SLFN11-deficient cells. The gene discussed is SLFN11; the disease is cancer.