Clerk et al. found that the hypertrophic agonists PE and endothelin 1 (ET-1) can activate Rac1 and then result in cardiac hypertrophy through regulation of ERK and probably JNK, but not p38; in addition, the upregulation of ERK activity and hypertrophy induced by these agonists are inhibited by Rac1(N17) [32]. This evidence concerns the gene MAPK8 and cardiac hypertrophy.