To date, >130 variants in both the regulatory and coding regions of UGT1A1 have been identified in hereditary hyperbilirubinemia patients [8], with variations identified in CN-I, CN-II, and GS reducing UGT1A1 enzyme activity to 0%, 10%, and 30%, respectively [9–11]. This evidence concerns the gene UGT1A1 and Hyperbilirubinemia.