Although JAK/STAT activation—particularly STAT3 phosphorylation in epithelial and fibroblast compartments—is demonstrable in IPF [209], it is not the dominant upstream driver, a role played instead by the TGF-β/SMAD, epithelial senescence, and epithelial stress pathways. The gene discussed is SOAT1; the disease is idiopathic pulmonary fibrosis.