Indeed, inactivating mutations of DMP1 result in autosomal recessive hypophosphatemic rickets (ARHR) in which primary overproduction of FGF23 by osteocytes leads to renal phosphate wasting, rickets and osteomalacia.21–23 In models of hereditary rickets, including DMP1 mutants, increased Fgf23 transcription results from paracrine activation of FGFR1,18,24 and downstream activation of the calcium-dependent NFAT signaling pathway.25 This evidence concerns the gene FGFR1 and autosomal recessive hypophosphatemic rickets.