DCLRE1A and cancer: Importantly, and unusually, their exonuclease activity can resect past site-specific crosslinks.10 Cells depleted in SNM1A and SNM1B show increased sensitivity to ICL-inducing agents including cis-platin and mitomycin C (MMC),11,12 which are routinely used as cancer chemotherapeutics.13 As such, compounds that inhibit SNM1A/B could potentiate the effect of these drugs or be useful in circumventing resistance to them.