However, a recent work in vivo in a transgenic mouse model of cardiomyocyte-targeted EGFR-deficient activation while confirmed the critical involvement of EGFR transactivation in A2-induced cardiac hypertrophy rejected it in cardiac hypertrophy due to MR activation.[19] The reason for this apparent discrepancy with our and others results are not clear at present. The gene discussed is EGFR; the disease is cardiac hypertrophy.