Indeed, it inhibits the expression of type IIa and IIc sodium‐phosphate cotransporters (NPT2a and NPT2c) on the apical membrane of proximal tubular cells, thereby blocking tubular phosphate reabsorption.[47, 48] It also inhibits the activity of 1α‐hydroxylase (CYP27B1) and stimulates the activity of 24‐hydroxylase (CYP24A1), leading to lower circulating levels of 1,25‐dihydroxyvitamin D.[49] Thus, FGF23 is considered as a potential candidate target for the treatment of XLHR. This evidence concerns the gene SLC34A3 and X-linked dominant hypophosphatemic rickets.