NGAL, usually recognized for its role in inflammation, is now highlighted as a key mediator in thrombosis and hemostasis. In deep vein thrombosis and hemostatic processes, NGAL drives hypercoagulability and promotes clot formation by binding to and enhancing the activities of thrombin, kallikrein, FXIa, and FVIIa while simultaneously inhibiting antithrombin. In addition, NGAL facilitates thrombin-induced platelet aggregation and boosts both the expression and activity of tissue factor on endothelial and monocyte surfaces, thereby initiating and sustaining the clotting cascade. See Figure 6K in the article by Xue et al that begins on page 975. Figure created with BioRender.com.