The transition of compensated hypertrophy to heart failure is accompanied by an increased expression of transforming growth factor β (TGFβ) [1,2] that contributes to cardiomyocyte apoptosis [3], enhanced β-adrenergic signaling [4] and contractile dysfunction [5,6,7], since overexpression of TGFβ in transgenic mice led to a moderate increase of myocardial β-adrenoceptor density and increased prohypertrophic signaling [1]. This evidence concerns the gene TGFB1 and heart failure.