AT is an important enzyme that inactivates thrombin,FXa, and to a lesser extent, FIXa, FXIa, and FXIIa.65 The activity of AT is further stimulated by heparan sulfate(an endogenous anticoagulant) and heparin derivatives.65 Therefore, targeting AT can enhance the activityof thrombin and FXa, potentially promoting hemostasis in patientswith hemophilia.66 Fitusiran is the firstsmall interfering RNA (siRNA) that specifically targets AT mRNA (mRNA)and induces its degradation primarily within hepatocytes (Figure 2).66,67. This evidence concerns the gene F10 and hemophilia.