A tight regulation of FGF23’s posttranslational modifications and processing is crucial, as mutations in modification sites and interference with processing can block or promote FGF23 cleavage, leading to elevated serum levels of intact FGF23 and hypophosphatemia (32, 38, 39) or to reduced serum levels of intact FGF23 and hyperphosphatemia (33, 34, 40–42), respectively, both associated with mineral bone disorders. The gene discussed is FGF23; the disease is hypophosphatemia.