The clinical data are sustained by in vitro results showing that neutrophils from MI patients with unfavorable evolution exhibit increased expression of pro-inflammatory molecules CCL3, IL-1β, IL-18, S100A9, and NETs, but also of molecules with essential roles in adverse progression post-MI: p22phox, Nox2, and metalloprotease MMP-9. This evidence concerns the gene CCL3 and myocardial infarction.