Lorentz et al found that mice treated with an anti-FXI antibody, 14E11, had decreased myocardial infarct size in a model of ischemia/reperfusion (I/R) injury, indicating that FXI activation or activity might contribute to cardiac I/R injury.41Kossmann et al revealed that depletion of FXI could not only decrease a vascular coagulation–inflammatory circuit in angiotensin II-induced arterial hypertension, but also prevent arterial hypertension-induced end-organ damage.42 The gene discussed is AGT; the disease is Hypertension.