SLC10A1 encodes the sodium-bile acid cotransporter (NTCP), which serves dual critical functions in hepatocytes. As its primary function, NTCP facilitates the hepatic uptake of bile acids from portal blood, acting as a basolateral transporter that maintains bile acid homeostasis 1. The protein demonstrates significant capacity for conjugated bile acid transport, with OATP1B3 showing similar taurocholate uptake capacity to NTCP 1. Additionally, SLC10A1 functions as the entry receptor for hepatitis B virus (HBV), with highly specific recognition properties 2. The transporter also facilitates uptake of other substrates including TRIAC (3,3',5-triiodothyroacetic acid), important for thyroid hormone analog transport 3. In hepatocellular carcinoma, SLC10A1 expression is significantly downregulated through epigenetic mechanisms, specifically loss of activating histone modification H3K27ac near the transcription start site 2. This downregulation contributes to cancer progression by disrupting adenosine metabolism through HIF1α pathways 4. SLC10A1 overexpression in hepatoblastoma cells reduces cell viability and promotes apoptosis 4. Disease associations include familial hypercholanemia type 2, and genetic variants may influence drug transport, including rifampicin pharmacokinetics 5. The protein's dual role in bile acid transport and viral entry makes it clinically significant for both metabolic liver diseases and HBV infection susceptibility.