Furthermore, cardiomyocyte death, cardiac hypertrophy, and heart dysfunction in CaMKII-δ9 tg mice were also ameliorated by z-VAD (Figures 2C–E), indicating that the cytosolic execution of apoptosis contributes to CaMKII-δ9-induced cardiomyocyte death, and cardiomyocyte death is essential for CaMKII-δ9-induced cardiomyocyte death, cardiomyopathy, and heart failure. This evidence concerns the gene CENPX and cardiomyopathy.