It was believed that AngII stimulated G-protein-dependent ERK1/2 activation through binding to AT1-R, but overexpression of AT1-R mutant lacking Gαq/Gαi coupling also induced ERK1/2 phosphorylation and developed severe myocardial hypertrophy both in vitro and in vivo [9], [10]. This evidence concerns the gene AGTR1 and cardiac hypertrophy.