Despite the rising prevalence of NASH, recommended treatment options are limited to dietary changes and exercise.[3, 38, 39] An abundance of potential pharmacological strategies are currently in development.[38] One approach is to interrupt the enterohepatic recirculation of bile acids to the liver by inhibiting the apical sodium-dependent bile acid transporter (ASBT).[40] The ASBT is a transmembrane protein localized on the luminal surface of ileal enterocytes. The gene discussed is SLC10A2; the disease is metabolic dysfunction-associated steatohepatitis.