This observation and previous findings that individuals and mice lacking BVRA activity are healthy [19,20,21,23], supports the idea that pharmacological inhibition of BVRA activity could be a valid approach to treat both the neonatal pathological unconjugated hyperbilirubinemia and the inherited severe form of Crigler-Najjar syndrome, reducing the risk of irreversible neurological damage. This evidence concerns the gene BLVRA and Crigler-Najjar syndrome.