In vivo, NMX treatment in a bleomycin-induced IPF model significantly reduced fibrosis, inflammation, and, critically, levels of phosphorylated STAT3 (p-STAT3), leading to the conclusion that NMX disrupts the STAT3/epithelial-mesenchymal transition (EMT) axis to restrict the myofibroblast pool. This evidence concerns the gene STAT3 and idiopathic pulmonary fibrosis.