In order to test the hypothesis that rapid progression of IPF might be a consequence of altered innate immune sensing and responsiveness to pathogen associated molecular patterns, we examined the relative levels of expression of TLR9 via quantitative PCR analysis in upper and lower lobe open lung biopsies obtained from patients with IPF compared with the histologically normal margins from resected lung tumors [1]. The gene discussed is TLR9; the disease is idiopathic pulmonary fibrosis.