STAT1 and STAT3 are phosphorylated in response to cytokines and angiotensin-II in cardiac myocytes [12,16] although STAT3 signaling is the principal mediator of pathophysiologic adaptation of the heart to circulating cytokines and is required for pathologic cardiac hypertrophy in response to angiotensin-II or pressure overload [13,17–20]. This evidence concerns the gene AGT and cardiac hypertrophy.