The advances that have been made over the last decade in microscopic, biochemical, molecular, and genetic techniques have led to substantial improvement in our understanding of platelet dense granule structure and function, and the implications of dense granule deficiencies for haemostasis. However, much has still to be learned. For example, what is the specific mechanism of docking and fusion that occurs during dense granule exocytosis? What are the roles of dense granule membrane proteins during exocytosis or after expression on the surface of activated platelets? Finally, how do the genetic defects identified in HPS and CHS result in the clinical phenotype of these diseases, and what does this tell us about the origin and function of the affected subcellular organelles?