Pulmonary tissue oxygen levels are difficult to quantify, but a role for hypoxia in the progression of pulmonary fibrosis has been supported by the observation that increased stabilisation of hypoxia-inducible transcription factor (HIF-1α) has been found in the lung tissues of IPF and cystic fibrosis patients and in mice with bleomycin-induced pulmonary fibrosis [2–4]. This evidence concerns the gene HIF1A and pulmonary fibrosis.