Pre-clinical studies demonstrated that healthy murine myocardium expresses low levels of OPN in response to increased afterload [6] and in human, increased plasma levels of OPN are associated with activation of the renin-aldosterone system and with myocardial and coronary microvascular damage in dilated cardiomyopathy [7] but it is still poorly defined whether its expression changes in failing heart of different origin. This evidence concerns the gene SPP1 and dilated cardiomyopathy.