Like mice and humans with XLH, mice overexpressing Fgf23 (32) and humans deficient in DMP1 (33) or ENPP1 (34, 35) have high circulating levels of FGF23, decreased 1,25D levels, and enthesopathy, further supporting our results that impaired 1,25D action as a consequence of high circulating levels of FGF23 underlies enthesopathy development in hypophosphatemic rickets. This evidence concerns the gene DMP1 and enthesopathy.