Olivier et al. (2016) and Vinholt et al. (2017) also found that TRAP-induced PA was enhanced in patients with cardiovascular diseases who were receiving dabigatran, and it was associated with an increased expression of thrombin receptors on the surface of platelets (Vinholt et al., 2017). On the other hand, rivaroxaban could contribute to attenuation of platelet activity and aggregation by inhibiting coagulation factor Xa, which is a factor that increases platelet activity likely via Protease Activated Receptor-1 (PAR-1) (Anand et al., 2018; Petzold et al., 2020). This evidence concerns the gene F2R and cardiovascular disorder.