By conducting molecular, immunohistochemical, and FCM analyses of IPF patients and murine specimens, they identified that PD-1+ CD4+ T cells (mainly Th17 subsets) promote pulmonary fibrosis via signal transducer and activator of transcription 3 (STAT3)-mediated IL-17A and transforming growth factor–β (TGF-β) production. This evidence concerns the gene IL17A and pulmonary fibrosis.