Similarly, the STAT2−/− hamster model established in this study exhibits a similar dysregulation of both the extrinsic (prothrombin elongation) and intrinsic (activated partial thromboplastin elongation) coagulation pathways upon infection, whereas IFNAR−/− mice only demonstrate increased clotting times for activated partial thromboplastin and no change in prothrombin clotting times34. This evidence concerns the gene IFNAR1 and infection.