To explore the complex role of multiple genetic modifiers on unconjugated neonatal hyperbilirubinemia, eleven common polymorphisms across five bilirubin metabolism genes [Heme oxygenase-1 (HMOX1), biliverdin reductase A (BLVRA), hepatic bilirubin-conjugating isoenzyme uridinediphosphoglucuronosyltransferase 1A1 (UGT1A1), and solute carrier organic anion transporter family member 1B1 (SLCO1B1) and 1B3 (SLCO1B3)] were determined in our case-control study of Chinese neonates. This evidence concerns the gene BLVRA and Hyperbilirubinemia.