Cardiomyocyte-specific deletion of the other major JAK protein in cardiomyocytes, JAK2, results in dilated cardiomyopathy [31] and treatment with a JAK2-specific inhibitor impairs STAT3 phosphorylation and increases apoptosis in rat hearts in response to acute myocardial infarction [8], indicating essential nonredundant functions for JAK2 signaling in cardiac homeostasis and adaptation to ischemic injury. This evidence concerns the gene STAT3 and dilated cardiomyopathy.