STAT3 and pulmonary fibrosis: On the other hand, STAT3 activation in fibroblasts has also been reported to promote fibroblast-to-myofibroblast differentiation, collagen deposition, and fibrosis [62–64]; hence, the possibility exists that the application of the SHP-1 agonist SC-43 may simultaneously target the STAT3/NFκB signaling in both the macrophages and fibroblasts, which are two of the most important cell populations for the pathogenesis of IPF, reshaping the immunofibrotic niche [65] and leading to the resolution of pulmonary fibrosis.