However, the concept of two separate (i.e., intrinsic and extrinsic) coagulation pathways is outdated and has been replaced by the cell-based TF-driven model of coagulation activation [2], and evidence is accumulating that indicates a role for FXII and FXI in the development of venous thromboembolism rather than physiological hemostasis [35]. The gene discussed is F11; the disease is venous thromboembolism.