Thrombosis, the localized clotting of blood, can occur in both arterial and venous systems, leading to significant medical consequences. Acute arterial thrombosis is a major cause of myocardial infarction and stroke, while venous thromboembolism is the third leading cause of cardiovascular-associated death. The pathogenic changes in blood vessels and blood that lead to thrombosis are not fully understood, and developing safer and more effective antithrombotic drugs remains a critical goal. Arterial thrombosis is primarily triggered by the rupture of atherosclerotic plaques, which release platelets that aggregate and form a thrombus. Platelet activation involves the cleavage of the PAR1 receptor by thrombin, leading to further platelet recruitment and thrombus growth. The coagulation cascade, initiated by tissue factor, generates fibrin, the main component of the thrombus. Antiplatelet drugs, such as aspirin and clopidogrel, target platelet activation and aggregation to prevent thrombosis. However, their main side effect is bleeding, limiting their use. Venous thrombosis is influenced by changes in blood composition, reduced blood flow, and alterations in the vessel wall. Anticoagulant drugs, such as vitamin K antagonists and heparins, target multiple proteases in the coagulation cascade to prevent thrombosis. New anticoagulants, like rivaroxaban, show promise in reducing the incidence of venous thromboembolism without increasing bleeding risk. Recent studies have identified new targets for antiplatelet and anticoagulant therapy, including cell-surface receptors and signaling pathways. For example, CD36, a scavenger receptor, and talin 1, a cytoskeletal protein, are potential therapeutic targets. Additionally, combination therapy and personalized medicine are emerging as promising approaches to improve the effectiveness and safety of antithrombotic treatments.Thrombosis, the localized clotting of blood, can occur in both arterial and venous systems, leading to significant medical consequences. Acute arterial thrombosis is a major cause of myocardial infarction and stroke, while venous thromboembolism is the third leading cause of cardiovascular-associated death. The pathogenic changes in blood vessels and blood that lead to thrombosis are not fully understood, and developing safer and more effective antithrombotic drugs remains a critical goal. Arterial thrombosis is primarily triggered by the rupture of atherosclerotic plaques, which release platelets that aggregate and form a thrombus. Platelet activation involves the cleavage of the PAR1 receptor by thrombin, leading to further platelet recruitment and thrombus growth. The coagulation cascade, initiated by tissue factor, generates fibrin, the main component of the thrombus. Antiplatelet drugs, such as aspirin and clopidogrel, target platelet activation and aggregation to prevent thrombosis. However, their main side effect is bleeding, limiting their use. Venous thrombosis is influenced by changes in blood composition, reduced blood flow, and alterations in the vessel wall. Anticoagulant drugs, such as vitamin K antagonists and heparins, target multiple proteases in the coagulation cascade to prevent thrombosis. New anticoagulants, like rivaroxaban, show promise in reducing the incidence of venous thromboembolism without increasing bleeding risk. Recent studies have identified new targets for antiplatelet and anticoagulant therapy, including cell-surface receptors and signaling pathways. For example, CD36, a scavenger receptor, and talin 1, a cytoskeletal protein, are potential therapeutic targets. Additionally, combination therapy and personalized medicine are emerging as promising approaches to improve the effectiveness and safety of antithrombotic treatments.