Contrarily, in MI patients, the same strategies could be used in an opposite fashion: administering mobilization factors with the aim of increasing levels of circulating EPCs (e.g., we found a strong positive correlation between plasma tenascin-C levels and circulating levels of KDR+CD133+ and CD133+ EPCs; should tenascin-C prove to act as a mobilization and/or homing factor to these EPCs, increasing the level of circulating and/or myocardial tissue tenascin-C could be beneficial to EPC mobilization and homing to hypoxic myocardial tissue). The gene discussed is KDR; the disease is myocardial infarction.