Recently, there is evidence that in fibroblasts of patients with IPF, TGF-β1 activates STAT3 signaling in a Smad2/3-dependent way, which is independent of JAK2; Liu-Ya Tang et al. found that JAK1, as a TGF βRI-interacting protein, can mediate TGF-β1, which induces early phosphorylation of STAT3 in a manner independent of Smad, thus promoting liver fibrosis [35]. The gene discussed is SMAD2; the disease is idiopathic pulmonary fibrosis.