In healthy individuals, TF-induced coagulation provides rapid clot formation followed by a secondary burst of thrombin generation via FXI. This secondary thrombin burst facilitates TAFI activation, which results in protection of the clot against premature lysis. In severe congenital hemophilia, the complete absence of FVIII leads to a triple defect: a delayed clot formation, an absent FXI-mediated secondary thrombin burst, and a consequently absent activation of TAFI. In contrast, acquired hemophilia is only a single coagulation defect with delayed clot formation but preserved secondary thrombin generation and TAFI activation. Professional illustration by Somersault18:24.