From these results we conclude that 1) reduced level of PTH in Fgf-23−/− mice could contribute to the upregulation of NaPi2a expression in these mice and thereby to the development of hyperphosphatemia, and 2) compensatory increased expression of NaPi2c cannot efficiently restore the effects of NaPi2a loss. This evidence concerns the gene SLC34A1 and hyperphosphatemia.