Having confirmed that increased bleeding in HHT patients is not due to coagulation alterations, and because dissecting other components of the hemostasis process in patients is not feasible due to ethical reasons, we decided to investigate it in murine genetic models of the disease: endoglin heterozygous mice (Eng+/−) for HHT-1 and Alk1 heterozygous mice (Alk1+/−) for HHT-2. Here, ENG is linked to hereditary hemorrhagic telangiectasia.