UGT1A1 and Hyperbilirubinemia: It was reported that a polymorphism of UGT1A1 gene promoter homozygous insertion of TA pairs (genotype UGT1A1*28/*28) might results in a decrease in bilirubin glucuronidation activity, leading to hyperbilirubinemia and late complication of patients with HS, such as development gallstones [34, 35].