UGT1A1 and Hyperbilirubinemia: The homozygous UGT1A1*28 polymorphism is often associated with GS, and similarly to GS patients, our patient had reduced UGT1A1 activity without complete cessation of enzyme activity.8 With the additional heterozygous UGT1A1 coding variant, we suspect that his intermediate degree of hyperbilirubinemia, between the reported average ranges for both CNS type 2 and GS, may reflect the cumulative effects of multiple UGT1A1 gene variants present.