PARP inhibitors are thought to become trapped at the sites of single-strand DNA breaks leading to double-strand DNA breaks when DNA replication is attempted.1 The double-strand DNA breaks would normally be repaired by the process of homologous recombination repair (HRR), which is a complex process including many proteins, notably BRCA1 and BRCA2. 2 Tumours with an HRR deficiency, such as those found in BRCA-mutated cancers, cannot accurately repair DNA damage when PARP protein function is also disrupted and both the base excision and HRR DNA repair pathways are rendered inoperative. This evidence concerns the gene BRCA2 and neoplasm.