To explain a possibly higher risk of myocardial infarction in dabigatran-treated compared with warfarin-treated patients, hypotheses have been raised for an augmented GP Ibα signaling downstream of von Willebrand factor binding [37], or enhanced platelet reactivity and increased platelet surface expression of PAR-1 and PAR-4 [18]. This evidence concerns the gene GP1BA and myocardial infarction.