The farnesoid X receptor (FXR) is a nuclear receptor and transcriptional regulator activated by bile acids or synthetic FXR agonists. FXR is expressed highly in the liver and intestine where modulation of FXR critically regulates the expression of genes involved in cholesterol and bile acid homeostasis, hepatic gluconeogenesis/lipogenesis, and inflammation. We review the roles of FXR and one of its intestinal target genes, fibroblast growth factor (FGF) 15 in mice/FGF19 in humans, play in regulating these important pathways in health and diseases. The main purpose of this review is to review therapeutics that target bile acid signaling to treat non-alcoholic steatohepatitis (NASH), a stage of disease within the spectrum of non-alcoholic fatty liver disease (NAFLD) with a focus on current preclinical studies in mice and clinical research. NASH is a huge medical burden and characterized by hepatic steatosis, inflammation, and progressive development of liver fibrosis. However, there is currently no Food and Drug Administration approved treatment option for NASH. While there are multiple factors contributing to NASH pathophysiology, bile acid regulation is proposed to have a major role in NASH pathogenesis. Synthetic FXR agonists and FGF19 protein may be promising agents to treat NASH, with obeticholic acid (OCA), cilofexor, tropifexor, nidufexor, EDP-305, and NGM282 currently in phase II or III clinical trials of NASH. FXR antagonism has also emerged, and antagonists like ursodeoxycholic acid (UDCA) and glycine-beta-muricholic acid (Gly-MCA) are in pre-clinical stage development for NASH treatment. This mini review seeks to evaluate and organize the literature available on FXR ligands and pathways for the treatment of NASH.