Considering the fact that hypoxia may promote ER stress in various organs17,18, and that the expression of the hypoxia-inducible factor 1α (HIF-1α) has been previously reported in AECs from IPF lungs19, we hypothesized that localized alveolar hypoxia and HIF-1α could be relevant stressors inducing prolonged ER stress and subsequent apoptosis of AECs in sporadic IPF. Here, HIF1A is linked to idiopathic pulmonary fibrosis.