GPBAR1-mediated β-catenin signalling also activated PI3K/AKT and inhibited the TLR4/NF-κB pathway, thus attenuating the inflammatory response, which suggests a new mechanism by which GPBAR1 regulates cholestatic liver disease in a model of cholestatic liver injury induced by BDL (Rao et al., 2020). Here, GPBAR1 is linked to Cholestatic liver disease.