Chronic hypophosphatemia is usually characterized by muscle weakness, fatigue, and the development of osteomalacia, accompanied by bone pain.(1) One of the major regulators of phosphate is fibroblast growth factor (FGF)23.(2) Recently it has been shown that FGF23 also interacts with iron metabolism and erythropoiesis.(3) The current case illustrates the interaction between FGF23 and iron status, and challenges the applicability of C‐terminal FGF23 (cFGF23) assays for the work‐up of hypophosphatemia in the setting of FGF23‐related disturbances. This evidence concerns the gene FGF23 and hypophosphatemia.