Given the fact that PARP-1 has ability to alter NF-κB activation and that several pro-inflammatory factors involved in COPD pathogenesis are dependent on activation of NF-κB, we speculate that decreased levels of TNF-α and IL-6 upon PARP inhibition as observed by Geraets et al. might be through suppression of NF-κB activation. The gene discussed is NFKB1; the disease is chronic obstructive pulmonary disease.