SLFN11 and cancer: This observation confirms the hypothesis that SLFN11 has a key role in replication stress and accumulation of damage during the S-phase.7,42 ATRi, WEE1i and CHK1i have also been described to modulate the replication stress response leading to increased genomic instability in specific sub-population of cancer cells.13,14,43 However, only modest resistance to monotherapy treatments with ATRi or CHK1i were observed in the absence of SLFN11, possibly because these agents did not lead to significant accumulation of DNA damage in the conditions we tested.