S100A9 and myocardial infarction: As shown in Figure 4A–F, the neutrophils isolated from MI patients with negative prognosis (MI_NP) exhibited increased gene expression of almost all analyzed pro-inflammatory mediators: CCL3, IL-1β, IL-18, S100A9, and of the intracellular cell adhesion molecule-1 (ICAM-1), which is known to mediate neutrophils infiltration in the infarcted area [13].