Neutrophils participate in the sepsis procoagulant phenotype; first, with the degradation of natural anticoagulants through the direct TM cleavage by neutrophil elastase, MPO and serine proteases [26] and, second, with the release of TF-positive microparticles and highly charged molecules such as H3, H4 and DNA [85], with activation of the extrinsic pathway of the coagulation cascade, leading to activated factor X formation and thrombin production [14,53]. Here, TF is linked to Sepsis.