Whereas hyperbilirubinemia induced by UGT1A1 deficiency appears largely responsible for early death, highly perturbed hepatic expression of genes involved in general cellular metabolic function, and notably those of starch, sugar and fatty acid metabolism was also observed in UGT1−/− mice, also supporting a contribution of UGT1A enzymes in those metabolic pathways (Nguyen et al., 2008). Here, UGT1A1 is linked to Hyperbilirubinemia.