Autosomal dominant hypophosphatemic rickets (ADHR) is a rare disease of the skeleton caused by mutations of the cleavage site of the fibroblast growth factor 23 (FGF23), causing an accumulation of the hormone. The disease has various clinical presentations and it has been observed an increase in FGF23 levels and consequent hypophosphatemia in association with iron depletion in both mouse models and human studies. The recent article by Imel and colleagues reported data from a pilot open-label study testing the hypothesis that iron supplementation could reduce FGF23 concentration in ADHR. Adult subjects with ADHR and baseline iron deficiency were treated with oral iron, whose dose was established based on the iron concentration and titrated and/or stopped accordingly in 12-month follow up protocol. Although only five subjects completed the protocol, the study provides interesting data on the efficacy of iron supplementation in reducing FGF23, whose levels normalized at 12 months in all cases. Additionally, authors observed an improvement in serum phosphate levels and hypophosphatemia-related symptoms, as well as discontinuation of calcitriol and phosphate supplementation during the study. Data from this study needs further validation by randomized trials including a larger number of patients of different ages. Many relevant aspects, particularly those related to the impact of iron supplementation on clinical symptoms and signs of the disease, need to be elucidated. Hence, the pilot study provides new interesting data for future management of ADHR, a rare disease in which only phosphate and calcitriol are currently approved for treatment of hypophosphatemia. Imel and colleagues propose that recognition and treatment of iron deficiency may have relevant clinical effects even beyond those related to restoration of the optimal iron state. Accordingly, iron supplementation in deficient ADHR patients may represent a valid and relatively low cost therapy to ameliorate hypophosphatemia.