Nevertheless, the complete rescue of Ugt1−/− mice from lethal hyperbilirubinemia by genetically blocking bilirubin production in the Bvra−/−Ugt1−/− mice, together with the absence of overt pathologies in middle-aged animals, provide strong experimental support to the postulate that inhibition of BVRA is a feasible option to treat severe unconjugated hyperbilirubinemia in both hyperbilirubinemic neonates and Crigler-Najjar syndrome patients. This evidence concerns the gene UGT1A1 and Crigler-Najjar syndrome.