UGT1A1 and Hyperbilirubinemia: For example, the activity of UGT1A1 conjugation in the tight control of bilirubin metabolism has established the importance of UGT1A1 genetic polymorphisms in the pathogenesis of toxic hyperbilirubinemias such as the Crigler-Najjar and Gilbert's syndromes in humans [75, 89, 94].