REV7/MAD2L2: the multitasking maestro emerges as a barrier to recombination

REV7/MAD2L2 plays important roles in translesion DNA synthesis and mitotic control. Two new papers extend its gamut by revealing its unexpected participation in pathway choice during DNA double-strand break repair. By inhibiting 5' DNA end resection downstream of 53BP1 and RIF1, REV7/MAD2L2 promotes non-homologous end joining at the expense of homologous recombination. Importantly, loss of REV7/MAD2L2 renders PARP inhibitors ineffective in BRCA1-deficient tumours, suggesting another possible mechanism for the acquisition of resistance to this important new class of drug.