Moreover, activated platelets secrete or generate agonists and cytokines, such as ADP, PF4, P-selectin, IL-1β, and vWF, which further amplify platelet activation and aggregation, fostering platelet–neutrophil interactions and NET formation, thereby fostering a proinflammatory and prothrombotic milieu during sepsis. This evidence concerns the gene PF4 and Sepsis.