Overexpression of cytokines such as IL-4, IL-6, IL-13, and TGF-β1 in ILD activates the JAK-STAT pathway, leading to macrophage activation with subsequent increased release of proinflammatory and profibrotic factors, and the differentiation of fibroblasts into myofibroblasts (Figure 2).69 Janus kinase-signal transducer and activator of transcriptions have indeed been found to be overexpressed in lung tissues of patients with ILD. This evidence concerns the gene SOAT1 and interstitial lung disease.