Overexpression of kinase-active TNNI3K in murine heart also resulted in pathological cardiac hypertrophy and cardiac dysfunction [3,17], conduction abnormalities [9], ischemia/reperfusion injury [7], and acceleration of cardiomyopathy in the pressure-overload model [14], suggesting that both an increase or a decrease in Tnni3k expression could result in cardiomyopathy pathogenesis. This evidence concerns the gene TNNI3K and cardiac hypertrophy.