However, altogether, our observations already appear to support our hypothesis of a link between FGF23 overproduction and hypophosphatemia, since (i) the complete etiological work-up did not reveal any other plausible causes, (ii) our results were supported by increased serum bio-intact FGF23 levels and the parallel favorable evolution of hepatic and biochemical parameters, and (iii) the liver expression of FGF23 was clearly induced in mouse models of acute hepatitis. This evidence concerns the gene FGF23 and hypophosphatemia.