CCL2-driven pro-inflammatorysignaling leads to a sustained increase in immune response in failingcardiomyocytes, resulting in further swelling, necrosis and thus an increasedrisk of death from heart failure; it has been reported that in animal models ofmyocardial infarction, blocking the CCL2/chemokine receptor 2 (CCR2) axis is effective in reduce infarctsize and protect surviving myocardium [37, 38]. The gene discussed is CCL2; the disease is infarction.