SNAI1 and pulmonary fibrosis: Comeglio et al. [13, 72] reported that TGF-β1, SNAI1, and SNAI2 expression levels substantially increase in the constructed rat model of pulmonary fibrosis, whereas, with the participation of FXR agonists (such as OCA), their expression levels are restored to those of the control group, thereby inhibiting the development of EMT.