The reduced production of myeloid chemoattractants induced by S100A9 inhibition provide important mechanistic support to our previous findings in a mouse model of MI in vivo, showing that treatment with ABR-238901 prevents neutrophil and monocyte migration from the bone marrow and spleen into the circulation, and recruitment into the heart (17, 39). The gene discussed is S100A9; the disease is myocardial infarction.