Of note, in another model of cardiac hypertrophy induced by aortic stenosis, Epac1 knockdown fails to prevent cardiac hypertrophy, but only fibrosis and cardiomyocyte apoptosis, suggesting that the cardioprotective effects of Epac1 deletion with respect to hypertrophy depend on the nature of stress [19]. This evidence concerns the gene RAPGEF3 and cardiac hypertrophy.