To determine the function of Pit1 and Pit2 in skeletal muscle independent of hypophosphatemia and the homeostatic endocrine changes resulting from hypophosphatemia, we generated a series of conditional knockout mice lacking one or two copies of Slc20a1 and Slc20a2 (smPit1−/−; smPit2−/− mice), using the postnatally expressed human skeletal actin (HSA)-cre. This evidence concerns the gene SLC20A1 and hypophosphatemia.