Elegant preclinical experiments led to the concept of synthetic lethality, which suggested that tumours without functional BRCA1 or BRCA2 protein would be more susceptible to PARP inhibitors compared with non-tumour tissues in the same patients.21 In this model, PARP inhibition leads to an accumulation of unrepaired single-strand breaks in DNA, which are converted to double-strand breaks when the tumour cell attempts DNA replication in the S-phase. Here, BRCA2 is linked to neoplasm.