A growing body of evidence suggested that genetic variants in uridine diphosphate glucuronosyltransferase 1A1 (UGT1A1), solute carrier organic anion transporter family members 1B1 and 1B3 (SLCO1B1, SLCO1B3), glucose-6-phosphate dehydrogenase deficiency (G-6-PD), heme oxygenase 1 (HMOX1), and biliverdin reductase A (BLVRA) are closely associated with the incidence of severe hyperbilirubinemia. Here, BLVRA is linked to G6PD deficiency.