However, we show that either HBMSCs self-secreting a high level of TGF-β1 or TGF-β1 added to CTD-UIP-HLFs can induce production of anti-fibrotic chemokine IP-10 [49–52], which may act downstream of TGF-β signaling to negatively regulate activation of myofibroblasts marker [53], leading to attenuation of α-SMA over expression in the treated CTD-UIP-HLFs. Here, ACTA1 is linked to idiopathic pulmonary fibrosis.