The protective effects of anti-GDF15 treatment in heart failure are in contrast to the findings that GDF15-deficient mice were more susceptible to cardiac rupture in a murine model of acute myocardial infarction.45,46 In a report by Xu et al.,47 genetic deletion of Gdf15 promoted LV hypertrophy and systolic dysfunction after transverse aortic constriction. This evidence concerns the gene GDF15 and hypertrophy.