It has been suggested that the FGF23 co‐receptor Klotho may have an FGF23‐independent role in the regulation of cardiac functions, protecting the heart from left ventricular hypertrophy and systolic dysfunction through regulation of TRPC6 channels in cardiomyocytes.34 However, in contrast to circulating FGF23, serum soluble Klotho was not found to be associated with left ventricular function or hypertrophy in human cardiology patients.36 Similarly, serum soluble Klotho remained unchanged in our murine and rat MI models. This evidence concerns the gene FGF23 and cardiac hypertrophy.