Variants in either an exon or the promoter of the UGT1A1 gene can result in UGT1A1 enzyme deficiency and impairment of bilirubin conjugation in hereditary unconjugated hyperbilirubinemia, which includes Gilbert syndrome (GS) and Crigler-Najjar syndrome (CNS).[2] GS and CNS were once considered to be distinct genetic and pathophysiological entities, although both are now attributed to mutations of UGT1A1, but with quantitatively different consequences.[3]. This evidence concerns the gene UGT1A1 and Gilbert syndrome.