Glanzmann thrombasthenia, first described in 1918 [1], is a severe, life-long bleeding disorder. The disease stems from a defect in platelet aggregation and manifests itself only in homozygotes while heterozygotes remain asymptomatic. The discovery of a deficiency of the glycoprotein (GP) IIb/IIIa complex in thrombasthenic platelets [2] provided a molecular basis of the disease. This GP complex functions in the presence of Cat as a receptor for fibrinogen, which under normal circumstances of platelet stimulation forms a bridge to adjacent platelets, thereby producing aggregates. Glanzmann thrombasthenia is heterogeneous. In 1972, Caen [3] described a milder form of the disease (type II) which could be distinguished from the more common type I by several clinical and laboratory features. It was subsequently shown that patients with type II disease have only a partial deficiency of the GP IIb/IIIa [4]. Recently, heterogeneity was found even among type I patients. Thus, the two GP may be present but with impaired function [5, 6] or, alternatively, residual amounts of either GP may be present [7].