PAR1 has a greater affinity for thrombinthan PAR4, but despiteearly clinical promise, the addition of vorapaxar (the only licensedPAR1 antagonist) to standard care failed to meet its primary efficacyoutcome in patients with acute coronary syndrome and was associatedwith an excess of major bleeding, especially intracranial hemorrhage,in phase 3 clinical trials.17,18 Therefore, attentionhas since turned toward PAR4 as a potential thrombin receptor therapeutictarget. This evidence concerns the gene F2R and acute coronary syndrome.