Cardiac hypertrophy, characterized by increased muscle mass accompanied by cell enlargement, is an essential compensatory response of myocytes to various pathophysiological insults including angiotensin II (Ang II).1, 2, 3, 4, 5 However, chronic progress to decompensated changes will eventually increase the risk of heart failure and sudden death.6, 7 Numerous mediators and signalling pathways have been found to be involved in the development of cardiac hypertrophy,1, 8, 9 but the underlying mechanisms contributing to the pathogenesis of cardiac hypertrophy still remain very elusive. Here, AGT is linked to heart failure.