This phenotype is similar to that observed in animals and humans with primary increases in FGF23,[27–29] and transgenic expression of either the full-length DMP1 or the C-terminal 57kDa DMP1 fragment reverses the excess FGF23 and osteomalacia present in the DMP1 null mice[9], suggesting that DMP1 acts to downregulate FGF23 expression. Here, FGF23 is linked to osteomalacia.