FDV is an inhibitor of OATP1B1, OATP1B3, UGT1A1, and MRP2, so FDV inhibits all steps of in vivo disposition of bilirubin and thus leads to benign accumulation of unconjugated bilirubin (Joseph et al., 2014; Wu et al., 2016; Huang et al., 2017; 2021); When FDV-mediated UGT inhibition is combined with predisposing genetics causing impaired bilirubin clearance, the incidence of benign hyperbilirubinemia (indirect bilirubin of >3.0 mg/dL) increases. This evidence concerns the gene SLC35A2 and Hyperbilirubinemia.