The inducers and mechanisms of FGF23 production and processing in bone are currently studied by many investigators [as reviewed in more detail elsewhere (48, 61–64)], and their characterization should provide important answers to one of the key questions in the field, i.e., why circulating FGF23 is elevated in CKD, as well as novel pharmacological targets to lower serum FGF23 levels. This evidence concerns the gene FGF23 and chronic kidney disease.