Bile acids are synthesized in the liver and secreted into the intestine to facilitate the absorption of lipophilic nutrients, with 95% of BAs being reabsorbed via the ASBT transporter.[5] Thus, the interruption of ASBT has been suggested as a promising strategy to attenuate bile acid‐related diseases.[50] Recently, the novel ASBT inhibitor A4250 has demonstrated promise in patients with progressive familial intrahepatic cholestasis.[51, 52] This study suggests that A4250 reduced CA levels and liver fibrosis progression in CCI4‐treated Slc27a5−/− mice. This evidence concerns the gene SLC10A2 and Hepatic fibrosis.