Treatment with RR-11a, a LGMN inhibitor, reduced TGF-β1 secretion from M2 macrophages, thereby diminishing communication between macrophages and fibroblasts and alleviating bleomycin-induced pulmonary fibrosis in mice.<h4>Conclusions</h4>Our research establishes a gene signature associated with MDMs, which may aid clinicians in the personalized management of IPF. The gene discussed is LGMN; the disease is pulmonary fibrosis.