Platelet reactivity is an important determinant of the risk of thrombosis and of the risks of ischaemic cardiovascular diseases such as heart attack and stroke. Over the last 15 years, genome-wide association studies of platelet reactivity phenotypes have reported approximately 50 genetic loci containing variants associated with platelet reactivity, implicating several genes in the molecular biology of platelet activation for the first time. Most of these studies have measured platelet reactivity using either light transmission aggregometry or flow cytometry. While informative, these phenotyping methods are costly, which has limited the sizes of platelet reactivity studies relative to those of other cardiovascular risk factors. Nevertheless, a recent approach in which platelet reactivity is predicted from haematology analyzer scattergram data has been applied to a large epidemiological cohort. The growing number of variants associated with platelet reactivity makes it possible to investigate the health consequences of modifying platelet reactivity through specific molecular mechanisms, using techniques such as Mendelian randomisation analysis. Such studies may point to drug targets for new antiplatelet therapies with better safety and efficacy profiles than existing agents.