In addition to the activation of FIX, X and V (step 1), we hypothesize that FXIa promotes thrombin generation by enhancing the TF-FVIIa pathway (step 2), including via the inactivation of TFPIα from platelets and TFPIβ from endothelial cells. Moreover, we hypothesized that in hemostasis, the main activator of FXI is thrombin (a), while in thrombosis the main activator of FXI is FXIIa (b).