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. Here, UGT1A1 is linked to Hyperbilirubinemia.