Long-term S100A9 blockade with ABR-238901 in mice with myocardial ischemia results in progressive left ventricular remodeling and gradual deterioration of cardiac function, indicating additional cardioprotective effects of S100A8/A9 by polarizing macrophages toward a reparative phenotype during the recovery phase post-MI. The gene discussed is S100A9; the disease is myocardial infarction.