A cell-based model of coagulation (see text for further explanation). Adapted from Jurlander B. Seminars in Thrombosis and Haemostasis. 27:373,2001. This model also is amenable to a tissue factor independent mechanism of thrombin generation in the absence of tissue factor and FVIII or FIX, such as would be the condition in severe congenital hemophilia A or B with alloantibody inhibitors or in acquired hemophilia with autoantibody inhibitors. In these situations According to the findings of Monroe et al.¹³ suprapharmacologic doses of rFVIIa can bind non-specifically to the activated platelet without the requirement of TF and subsequently can activate factor X to Xa in the absence of factor VIII or IX. In contrast, the Mann model¹⁴ suggests that suprapharmacologic doses of rFVIIa activates coagulation by overcoming an intrinsic inhibition of zymogen FVII in the absence of TF.