In as much as bacterium–platelet interactions are central to the pathogenesis of infective endocarditis, we examined the influence of the GPIIIa PlA1/A2 and the FcγRIIa H131R platelet receptor polymorphisms on S. aureus-induced platelet adhesion, activation and aggregation in vitro and clinical outcome in patients with infective endocarditis. This evidence concerns the gene POU2F3 and infective endocarditis.