However, given that fibrosis severity is the strongest predictor of liver-related outcomes in MASH patients, that many investigational therapies have failed to meet fibrosis-related endpoints, and that all FXR agonists, tropifexor, and cilefexor ameliorate liver fibrosis, a likely scenario could be the development of combinatorial therapies to treat fibrosis and steatosis in MASH patients. The gene discussed is NR1H4; the disease is metabolic dysfunction-associated steatohepatitis.