However, genetic inhibition of cardiac ERK1/2 promotes stress‐induced apoptosis and heart failure but has no effect on hypertrophy in vivo,48 and ERK1/2 pathway is reported to activate the transcription of several key fibrotic genes through TGFβ‐Smad pathway,29 indicating that ERK1/2 may not be necessary for cardiac hypertrophy but play an important role in promoting fibrosis. This evidence concerns the gene MAPK3 and heart failure.