Cells with defective homologous recombination (HR) due to mutation of the BRCA1 or BRCA2 genes are hypersensitive to the inhibition of poly-ADP ribose polymerase-1 (PARP-1).1,2 This led to the clinical development of PARP inhibitors as the first class of cancer therapeutics targeted against a DNA repair process.3 The gene discussed is PARP1; the disease is cancer.