UGT1A1 and Crigler-Najjar syndrome: Its activity can lead to indirect hyperbilirubinemia, which is associated with many hereditary hyperbilirubinemic conditions such as Gilbert or Crigler-Najjar syndrome.[18] Although Gilbert syndrome is often described as a benign laboratory finding, it may alter drug metabolism by decreasing the ability to conjugate drugs.[19] Nilotinib-induced hyperbilirubinemia has been reported to be mainly related to the decrease in UGT1A1 activity [20–23] (Table 1).