Therefore, it is suggested that HIF1α may be one of the mediators of increased FGF23 in iron deficiency, anemia, or inflammation even though HIF1α does not appear to be a necessary factor for FGF23 expression since the knockout of HIF1α in mature osteoblasts does not affect FGF23 levels in wild-type mice or those with XLH [114]. Here, FGF23 is linked to X-linked hypophosphatemia.