However, this increase in FGF23 production only results in the accumulation of intact FGF23 levels and hypophosphatemia in ADHR patients or in mice with an ADHR-like mutation in Fgf23. In wildtype animals or healthy subjects, the same stimuli result in increased circulating levels of cleaved FGF23, revealing the importance of endoproteolysis by PC for the regulation of this hormone. This evidence concerns the gene FGF23 and hypophosphatemia.