UGT1A1 and Hyperbilirubinemia: Moreover, nilotinib is not a substrate for uridine diphosphate glucuronosyltransferase 1A1 (UGT1A1) enzymes, but an inhibitor of human UGT1A1 in vitro[13], and CML patients with the UGT1A1*28 polymorphism show an increased risk of nilotinib-induced hyperbilirubinemia [14].