However, recent studies using mouse models of FGF23 knockout and upregulation do not support this supposition,26, 27 and individuals with primarily FGF23‐related hypophosphatemic bone disease do not consistently present with ventricular hypertrophy.28 As with CKD, the difference may be due to whether elevations of FGF23 are occurring during hyperphosphatemia or hypophosphatemia. Here, FGF23 is linked to cardiac hypertrophy.