REV 7/ MAD 2L2: the multitasking maestro emerges as a barrier to recombination

REV 7/ MAD 2L2 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 53 BP 1 and  RIF 1, REV 7/ MAD 2L2 promotes non‐homologous end joining at the expense of homologous recombination. Importantly, loss of REV 7/ MAD 2L2 renders PARP inhibitors ineffective in BRCA 1‐deficient tumours, suggesting another possible mechanism for the acquisition of resistance to this important new class of drug.