To differentiate RA-ILD from other common pulmonary fibrosis and to be in line with the highly mixed background of inflammation and fibrosis in RA-ILD disease, we combined the abnormal elevation of IL-1β and TGF-β in an animal model, and the combined induction of human embryonic lung cells can better simulate the disease environment of RA-ILD in a human environment. This evidence concerns the gene IL1B and rheumatoid arthritis.