The pathogenesis of HIT mainly involves the binding of heparin to platelet factor 4 (PF4) to form a heparin-PF4 complex that stimulates the body to produce anti-PF4/heparin antibodies and mediates an immune response, which leads to platelet activation and reduction and results in an elevated risk of thromboembolic disease [4]–[6]. Here, PF4 is linked to Thromboembolism.