QPD is associated with proteolytic degradation of stored alpha-granule proteins due to intraplatelet activation of the fibrinolytic cascade, without evidence of systemic fibrinogenolysis [4, 7, 8, 12] and mice genetically engineered to overexpress uPA in megakaryocytes have a QPD-like bleeding disorder [14]. The gene discussed is PLAU; the disease is hemorrhagic disease.