FGF23 is inactivated by proteolytic cleavage at aconserved furin cleavage site within the FGF23 protein, which is mutated in ADHR patients.In subjects with normal kidney function, increased blood concentrations of intact FGF23 leadto renal phosphate wasting and subsequently impaired bone mineralization. This evidence concerns the gene FGF23 and autosomal dominant hypophosphatemic rickets.