Given that bone is the source of FGF23 in both physiologic and pathologic conditions such as fibrous dysplasia (FD) (19–21) and that the vast majority of patients with extensive EN or GCMN caused by the same gain-of-function RAS mutations do not have hypophosphatemia (22, 23), we postulate that dysplastic bone is the tissue source of the “phosphaturic substance” proposed by Aschinberg et al. and now identified as FGF23. This evidence concerns the gene FGF23 and Fabry disease.