The increase in FVIII:C was mainly seen in a hypercoagulable state and thrombotic disease,[10–12] and the lack of AT-III and AT may lead to thrombosis.[13,14] PC and PS activity increased to inhibit the coagulation process by inactivating VIIIα and Vα.[15,16] Plasminogen will be activated to produce plasmin by tPA and uPA, which play an important role in physiological hemostasis and thrombus degradation.[17,18] The increase in tPA and uPA activity and decrease in PAI1 activity led to the decrease in plasminogen, the production of plasmin, and the decrease in antiplasmin level. This evidence concerns the gene PLAT and thrombotic disease.