SLC10A2 (ASBT) is an apical sodium-dependent bile acid transporter that mediates the reabsorption of conjugated and unconjugated bile acids from the small intestine lumen 123. It functions as a non-covalent homodimer or higher-order oligomer 4 and operates collaboratively with other transporters to enable enterohepatic circulation and bile acid recycling 5. Beyond intestinal absorption, SLC10A2 demonstrates metabolomic footprints consistent with kidney-mediated bile acid reabsorption 6. SLC10A2 expression is regulated by multiple transcription factors and nuclear receptors. The glucocorticoid receptor transactivates the human ASBT promoter 7, while peroxisome proliferator-activated receptor alpha (PPARα) provides an additional regulatory mechanism linking bile salt absorption to hepatic lipid metabolism 8. The histone demethylase KDM6B directly activates SLC10A2 transcription 9. Genetically, reduced SLC10A2 expression occurs in Crohn's disease patients and correlates with bile acid malabsorption 7. Beyond intestinal disease, SLC10A2 serves as a therapeutic target in colorectal cancer through immunomodulation of myeloid-derived suppressor cells 9 and in non-small cell lung cancer via PPARγ/PTEN/mTOR signaling 10. ASBT inhibitors represent promising therapeutic agents for liver, gallbladder, intestinal, and metabolic diseases 11.