Thus, it is suggested that about 60% reduction of the intact Fgf23 in Galnt3−/− mice resulted in hyperphosphatemia and hypercalcemia without an increase of serum level of 1,25(OH)2D3 and without a severe reduction of PTH and led to the accelerated mineralization of osteoid, which inhibits cleavage of type I collagen, and finally to the increase of the trabecular bone volume under the normal bone turnover. This evidence concerns the gene GALNT3 and hypercalcemia disease.