Although the mechanism by which AVP deficiency (NIL-induced) causes hyperbilirubinemia is not known, a possible explanation for this may be that AVP in the liver is involved in hepatocyte ureogenesis, glycogenolysis, neoglucogenesis, and cell regeneration through its V1a receptors [41], while the V2 AVP receptors regulate the biliary epithelium functions [42]. This evidence concerns the gene AVP and Hyperbilirubinemia.