In 2016, according to the prognostic role of FVIIa–AT in our cohort of patients with clinically stable CAD, we hypothesized the possible beneficial use of oral direct FXa inhibitors in patients with high FVIIa–AT levels, by blocking the excess of FX activation mediated by the FVIIa–TF pathway [31]. Here, F10 is linked to coronary artery disorder.