These data are consistent with those of a study conducted on patients with atrial fibrillation, showing a significant reduction in 11-dehydro-TXB2, the main urinary metabolite of TXB2, in patients treated with rivaroxaban and apixaban compared with warfarin [42]; that finding was related to the shedding of soluble GPVI, letting the authors postulate a further mechanism of antiplatelet effect by FXa inhibition. Here, F10 is linked to atrial fibrillation.