Pharmacological inhibition of PARP-1 provides protection from oxidative stress-associated tissue injury, down-regulates the inflammatory response and is also beneficial in cancer treatment by mechanisms such as selective killing of homologous recombination-deficient tumor cells, down-regulation of tumor-related gene expression (e.g. AP-1 and NF-κB-mediated transcription) and apoptotic threshold in the co-treatment with chemo and radiotherapy48. The gene discussed is NFKB1; the disease is cancer.