Observations in rodents indicate that ROCK contributes both to myocardial fibrosis and cardiomyocyte apoptosis.18 ROCK1 activation by caspase‐3 plays an essential role in cardiomyocyte apoptosis.19 In a transgenic mouse model of dilated cardiomyopathy, ROCK1 deletion attenuated left ventricular dilation, contractile dysfunction and cardiomyocyte apoptosis20 and cardiomyocyte‐specific ROCK1 overexpression accelerated progression to HF by increasing apoptosis and fibrosis.21 These studies strongly suggest that ROCK activation may promote myocardial apoptosis in human HF as well. This evidence concerns the gene ROCK1 and hydrops fetalis.