1,25(OH)2D3, primarily produced in the kidneys, exerts its effects through the vitamin D receptor (VDR), which is most abundantly expressed in tissues involved in the maintenance of mineral and bone homeostasis, such as the parathyroid glands, intestine, kidney, and bone.(1) Mutations in the VDR gene that result in a defective receptor lead to the development of vitamin D‐dependent rickets type 2, an autosomal recessive disorder characterized by the early onset of rickets, hypocalcemia, secondary hyperparathyroidism, and hypophosphatemia.(2). This evidence concerns the gene VDR and hypophosphatemia.