Cardiac-specific over-expression of Mst1 in mouse results in activation of caspases, increased apoptosis and dilated cardiomyopathy, whereas the inhibition of endogenous Mst1 prevents apoptosis of cardiomyocytes and cardiac dysfunction after myocardial infarction without producing cardiac hypertrophy [62,64]. This evidence concerns the gene MST1 and cardiac hypertrophy.