Hyperphosphatemia is only seen in older, more slowly or non-growing Fgf23/VDR compound mutant mice beyond 3 months of age (30, 47), suggesting that the phosphaturic effect of FGF23 is physiologically less essential compared with the 1α-hydroxylase-suppressing effect, at least in mice. This evidence concerns the gene FGF23 and hyperphosphatemia.