EGFR and cardiac hypertrophy: 2) The demonstration of a key role played by the transactivation of the epidermal growth factor receptor (EGFR): The finding by Sadoshima’s group that A2, probably the most widely accepted hypertrophic agent, failed to induce cardiac hypertrophy in transgenic mice overexpressing a mutant AT1 receptor lacking EGFR transactivation in the myocardium [7], lead us to speculate that the SFR, as a result of the myocardial stretch-triggered signalling pathway, would be probably abolished by preventing EGFR transactivation.