Similarly, the NF-κB signaling pathway mediates interactions between endothelial cells, platelets, and inflammatory responses, which disrupts coagulation-fibrinolysis homeostasis and induces deep vein thrombosis, and we hypothesize that NF-κB is also a mediator of TNFSFS12-induced VTE [56]. This evidence concerns the gene NFKB1 and deep vein thrombosis.