Though the exact mechanism of FCM‐associated HPP is unknown, a hypothesis is that in the clinical setting, FCM prevents the cleavage of iFGF23 to the C‐terminal FGF23 (cFGF23) and N‐terminal FGF23 (nFGF23), resulting in increased circulating iFGF23 levels, which in turn cause lower serum phosphate levels (Figure 1), similar to genetic diseases of primary FGF23 excess (autosomal dominant hypophosphatemic rickets) or tumor‐induced osteomalacia [20, 21, 22]. Here, FGF23 is linked to autosomal dominant hypophosphatemic rickets.