An absence of PAR4 in mouse models results in impaired hemostasis and a protection against pulmonary embolism,9 and a small number of missense coding variants in F2RL3 that alter platelet aggregation and function have been described.10–12 In particular, the Thr120 variant of the common single nucleotide polymorphism (rs773902) has been highlighted as functionally relevant13–15 providing a link between PAR4 and the heritable interindividual variation in platelet reactivity. This evidence concerns the gene F2RL3 and pulmonary embolism.