Therefore, as GPIIb/IIIa-mediated outside-in signaling serves as a regulating point not only for consolidating aggregation but also for limiting further platelet activation and calcium entry [49,50], a missing inhibitory mechanism (due to lack of the receptor) could explain a higher calcium influx in GT patients and in turn regulate the calcium influx in individuals not affected by GT. This evidence concerns the gene ITGA2B and Glanzmann thrombasthenia 1.