The discovery more than 15 years ago of a synthetic lethal (SL) relationship between mutations in the breast cancer susceptibility, tumour-suppressor genes BRCA1 and BRCA2 and the inhibition of poly(ADP-ribose) polymerase (PARP) enzymes [1,2] spearheaded the clinical development of PARP inhibitors (PARPi). The gene discussed is BRCA2; the disease is neoplasm.