Then we established a knock‐in XLHR mouse model by first introducing the c.T1349C variant into mice using CRISPR/Cas9 technology and our in vivo results demonstrated that typical XLHR clinical manifestations occurred in a gene‐dosage manner, including growth retardation, skeletal dysplasia (rickets/osteomalacia), and hypophosphatemia, together with elevated serum FGF23 and ALP. Here, FGF23 is linked to osteomalacia.