In contrast, in a mouse model of chronic kidney disease, Kawakami et al. showed that FGF23 increased both parathyroid cell proliferation and PTH release, and both effects were blocked in mice with parathyroid-specific conditional knockouts (cKO) lacking either α‐Klotho and/or FGFR1-4 [11]. Here, FGF23 is linked to chronic kidney disease.