Pathophysiologically, PLT hyperactivity and hyper-aggregation can occur when levels of stimuli, such as those of thromboxane A2 (TXA2), Col, or ADP, are below a certain threshold for full, irreversible PLT aggregation, while increased vWF levels can lead to hypercoagulability in patients with thalassemia, particularly in splenectomized cases [22]. The gene discussed is VWF; the disease is thrombophilia.