PROCR and thalassemia: Since EPCR EVs are known to preserve functional anticoagulant activity (Perez-Casal et al., 2005; Morel et al., 2009), we postulated that the reduction in the number of EPCR-labeled EVs observed in thalassemic patients can lead to altered hemostatic balance of the activated protein C system, acting as an additional inductive factor of hypercoagulable state in thalassemia patients.