Notably, cardiomyocyte-specific ROCK1 deficiency promotes pressure overload-induced cardiac hypertrophy and fibrosis, whereas cardiomyocyte-specific ROCK2-deficient mice show alleviation of cardiac hypertrophy and fibrosis under exposure to pressure overload, suggesting that inhibition of ROCK1 is not a suitable therapeutic strategy for heart failure [32]. This evidence concerns the gene ROCK2 and heart failure.