Of note, rescue experiments confirmed that inhibiting or continuously activating Rac1 could not only completely reverse the effects of DEF6 overexpression or silence on the phenotype of cardiomyocyte hypertrophy and the activity of MEK-ERK1/2 signaling, but also created addition effects compared to basic condition, suggesting that Rac1 activation is necessary and sufficient for the development of pathological cardiac hypertrophy. This evidence concerns the gene RAC1 and cardiac hypertrophy.