The partial improvement of left ventricular ejection fraction in the mtCaMKII x AC3-I interbred mice suggested that mitochondrial and extramitochondrial CaMKII each have the potential to decrease myocardial function, but the unchanged end-diastolic volumes indicate that mitochondrial CaMKII exclusively promotes dilated cardiomyopathy, and not myocardial hypertrophy. This evidence concerns the gene ADCY3 and dilated cardiomyopathy.