All this makes the perfect environment for D. desulfuricans to thrive, producing H2S that not only can be toxic for the epithelial barrier [47] but can also modulate the hepatic bile acid metabolism by induction of the farnesoid X receptor (FXR) and inhibition of cholesterol 7 alpha-hydroxylase (CYP7A1), to produce more hydrophobic bile acids due to increased deoxycholic acid (DCA) and decreased β-muricholic acid (βMCA), eventually giving place to hepatic and biliary cholesterol overloading and even promoting gallstone formation [48]. Here, NR1H4 is linked to gallstones.