Treatment of homologous recombination-deficient tumours with PARP inhibitors, particularly those with BRCA1 or BRCA1 mutations, generates significant levels of DNA damage however (Farmer et al, 2005), and there may be a threshold above which the DNA damage-induced stress signals overwhelm the otherwise anti-inflammatory effects of PARP inhibition. The gene discussed is PARP1; the disease is neoplasm.