Therefore, the increase of platelet-neutrophil adhesion observed in our study at later time-points after mTPOR-MBP administration may reflect the inhibition of platelet activation and adhesion to leukocytes and, consequently, of platelet-neutrophil aggregates to the endothelium, which may be implicated in the protective effect of TPO blockade on inflammation- or sepsis-induced organ-damage. The gene discussed is MBP; the disease is Sepsis.