We and others also reported that DMP1 mutations are responsible for autosomal recessive hypophosphatemic rickets (ARHR) in human patients, including bone defects and an increase in fibroblast growth factor 23 (FGF-23) levels (although some of DMP1 mutation patients overlapped with the normal range for FGF-23).(12–14) However, there is a phenotypic difference between human patients (mild) and Dmp1-null mice (severe). This evidence concerns the gene FGF23 and autosomal recessive hypophosphatemic rickets.