SLC10A1 encodes the sodium/taurocholate cotransporting polypeptide (NTCP), a liver-specific transporter that removes bile salts from circulation and maintains bile acid homeostasis 1. The protein contains nine membrane-spanning or membrane-associated segments and exhibits high affinity for taurocholate, with an apparent Km of 6 microM 12. SLC10A1 expression is regulated by liver-enriched transcription factors, particularly C/EBP, which binds to elements in its TATA-less promoter 3. Beyond bile acid transport, SLC10A1 serves as the primary hepatocyte receptor for hepatitis B virus (HBV) entry, with highly specific recognition 4. During hepatocellular carcinoma development, hNTCP expression is downregulated through epigenetic silencing—specifically, loss of the activating histone modification H3K27ac at the transcription start site 5. Restoring this modification with histone deacetylase inhibitors can reactivate hNTCP expression and render cancer cells susceptible to HBV infection 5. Loss-of-function mutations and reduced expression of SLC10A1 are associated with familial hypercholanemia and intrahepatic cholestasis. Clinically, entry inhibitors targeting NTCP—including bulevirtide, bulevirtide acetate, myrcludex B, and hepalatide—are used to prevent HBV infection and treat chr14 hepatitis B virus infection. Additionally, overexpression of SLC10A1 suppresses hepatocellular carcinoma cell proliferation, migration, and aerobic glycolysis 6, suggesting a protective role against HCC progression.