Since only some of these animal models develop kidney injury, hyperphosphatemia, or hypertension, while all of them have elevated FGF23 and cardiac hypertrophy, one can assume that by directly targeting the myocardium, FGF23 is a major driver of cardiac remodeling that acts independently of other pro-hypertrophic factors, such as high blood pressure or uremic toxins. This evidence concerns the gene FGF23 and cardiac hypertrophy.