The isolated 72‐residue‐long C‐terminal tail of FGF23 (180‐251) has previously been shown to interfere with FGF23 signaling by competing with the full‐length ligand for binding to the FGFR‐Klotho complex, suggesting the possibility that it may serve as a potential therapeutic for the treatment of XLHR.[36] Therefore, we constructed an MC‐DNA vector expressing MC.CMV‐FGF23 (180‐251) and delivered it to Phex‐T1349C mice at 4 weeks of age via a single intramuscular injection (Figure 6A). Here, FGF23 is linked to X-linked dominant hypophosphatemic rickets.