The FDA-approved small-molecule antagonist, vorapaxar, effectively and irreversibly inhibits various downstream signaling pathways of PAR1; however, its usage is limited due to the increased risk of bleeding and intracranial hemorrhage.18–21 To avoid the disadvantage of the orthosteric antagonist, an increasing number of allosteric modulators, including parmodulins and pepducins, are designed to target the intracellular domain of PAR1,22–25 with the aim of disrupting or inhibiting G protein binding. The gene discussed is F2R; the disease is intracranial hemorrhage.