ACTA1 and idiopathic pulmonary fibrosis: This study examined the paradox of the TGF-β1 pro-fibrotic factor in stimulating α-SMA expression and myofibroblast differentiation and showed that excessive TGF-β1 secretion from MSC cells increased IP-10 levels in UIP-HLF (Usual interstitial pneumonia- human primary lung fibroblasts) and the simultaneous decrease in α-SMA expression (93).