Experimentally, both in vitro and in vivo studies support a role for KLF15 as a repressor of pathological cardiac hypertrophy and fibrosis [11–13] which occurs through inhibition of the activity of two pivotal pro-hypertrophic transcriptional regulators, GATA binding protein 4 (GATA4) and myocyte enhancer factor 2 (MEF2) and their effects on the atrial natriuretic peptide (ANP) and brain natriuretic peptide (BNP) promoters [11]. Here, MEF2A is linked to cardiac hypertrophy.