Ali MK, Kim RY, Brown AC, et al. - Researchers explored the impacts of iron accumulation on the pathogenesis of pulmonary fibrosis and associated lung function decline applying a combination of murine models of iron overload and bleomycin‐induced pulmonary fibrosis, primary human lung fibroblasts treated with iron, and histological samples from patients with or without idiopathic pulmonary fibrosis (IPF). It was indicated that iron levels are significantly raised in iron overloaded transferrin receptor 2 mutant mice and homeostatic iron regulator gene–deficient mice and this is correlated with increases in airway fibrosis and decreased lung function. These experimental and clinical data indicate that raised accumulation of pulmonary iron plays a key role in the pathogenesis of pulmonary fibrosis and lung function decline. Moreover, the evidence indicates the potential for the therapeutic targeting of increased pulmonary iron in the treatment of fibrotic lung diseases such as IPF.