S100B and myocardial infarction: In particular (i) in rat model of myocardial infarction it has been shown that S100B may play a dual role in cardiomyocytes survival or death (i.e., necrosis and apoptosis) through a RAGE-dependent mechanism, and (ii) S100B, once released from damaged myocytes, with consequent leakage of the protein into the systemic circulation, is approximately 1000-fold less than the amount of protein required to induce apoptosis [38].