Increased FGF23 activity may depend on (i) an abnormal overexpression, as in the case of the rare tumor-induced osteomalacia; (ii) specific pathogenic variants in the FGF23 gene leading to mutant proteins that are resistant to enzymatic processing; and (iii) impaired FGF23 degradation due to partial or full deficiency of the phosphate-regulating endopeptidase homolog X-linked (PHEX) gene product [4]. The gene discussed is FGF23; the disease is osteomalacia.