Our finding that PAR-1 deficiency improves survival early in severe murine pneumococcal pneumonia is in accordance with data by Niessen et al, who, using a PAR-1 antagonist, showed that functional PAR-1 reduces survival in polymicrobial sepsis induced by CLP, a finding which was associated with dendritic cell-mediated sustainment of proinflammatory and procoagulant mechanisms [11]. This evidence concerns the gene F2R and pneumococcal pneumonia.