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]. The gene discussed is VWF; the disease is myocardial infarction.