We show for the first time that the STING pathway is activated in the lung of ILD patients, as seen by STING overexpression, phosphorylation and dimer formation, TBK1 and IRF3 phosphorylation, and downstream CXCL10 production (Fig. 2c–e), correlating with epithelium damage (Fig. 2f). This evidence concerns the gene STING1 and interstitial lung disease.