In the Dmp1-null mouse model of ARHR, genetic overexpression of a Dmp1 transgene fully rescues FGF23 levels, hypophosphatemia, and bone defects (21, 34–36), but studies specifically targeting FGF23 in models of ARHR are scarce. This evidence concerns the gene FGF23 and autosomal recessive hypophosphatemic rickets.