In fact, OATP1B1/B3 had the main function of transporting DBIL,28 and hypercholanemia reportedly resulted in reduced expression of OATPs in the basolateral membrane of the hepatocyte in mice,5 hence impairing the hepatocytic uptake of DBIL from plasma and giving rise to direct hyperbilirubinemia (cholestasis). This evidence concerns the gene SLCO1B1 and cholestasis.