On this basis, since the main function of OATP1B1/B3 is to uptake plasma bilirubin (including DBIL and IBIL) besides bile acids,28 hypercholanemia in NTCPD competitively inhibited the transport of bilirubin by OATPs and hence gave rise to neonatal indirect hyperbilirubinemia.10 This evidence concerns the gene SLCO1B1 and Hyperbilirubinemia.