SLC10A5 is a solute carrier family 10 member localized to the plasma membrane that functions in bile acid uptake and homeostasis. As an orphan transporter within the SLC10 family, SLC10A5's specific substrate remained unknown until recently 1, though it shares structural similarity with bile acid transporters 2. Recent evidence demonstrates that SLC10A5 mediates sodium-dependent bile acid transport; SLC10A5 deficiency impairs hepatocyte bile acid uptake and causes hypercholanemia, characterized by elevated serum and hepatic bile acids 3. Loss of SLC10A5 function downregulates expression of bile acid synthesis regulators (FXR and SHP) while upregulating synthesis genes (CYP7A1 and CYP8B1), indicating disrupted negative feedback control of bile acid production 3. SLC10A5 exhibits both homodimerization and heterodimerization with other SLC10 family members, a feature that may regulate its transport function 4. Clinically, heterozygous SLC10A5 mutations (c.994_995del, p.D332X) have been identified in patients with elevated serum bile acids and altered bile acid profiles, establishing a disease-relevant role in cholestasis pathogenesis 3. SLC10A5 is highly expressed in liver and kidney, tissues critical for bile acid metabolism and excretion 1.