Radiation-induced pulmonary fibrosis constitutes a major adverse effect of thorax irradiation that develops 6 to 24 months after radiation therapy, with symptoms ranging from nonproductive cough and dyspnea to respiratory insufficiency in severe cases. A sophisticated network between resident cells, immune cells, and soluble mediators leads to the observed fibrotic alterations of the lung tissue. In a preclinical murine model, it was found that CD73-generated adenosine plays an active role in the pathogenesis of radiation-induced lung fibrosis driving excessive tissue remodeling. Targeting the CD73/adenosine axis reduced pathological fibrosis development, suggesting new routes for therapeutic intervention. For details, see article by Wirsdörfer and colleagues on page 3045.