Our previous work demonstrated that both bone FGF23 and DMP1 expression are elevated in CKD patients; the expression of these proteins correlate directly with each other and higher expression of both proteins is associated with decreased osteoid accumulation (i.e. improved mineralization).[2] The finding that higher expression of FGF23 and DMP1 is related to improved indices of skeletal mineralization appeared contradictory to data from animals and humans with normal kidney function, leading us to postulate that although DMP1 expression is upregulated in CKD, its function is likely impaired. This evidence concerns the gene FGF23 and chronic kidney disease.