ABL1 and Hyperbilirubinemia: The inhibition of UGT1A1 may lead to accumulation of bilirubin to toxic levels, which may be the mechanism of atazanavir-, indinavir-, erlotinib-, and nilotinib-related hepatic toxicities (eg, jaundice and hyperbilirubinemia).47,48,49 Further studies will be needed to investigate the mechanism of BCR-ABL TKIs–associated hepatotoxicity.