Experimental in vivo models of DVT implicate a complex interplay between activated endothelium (P-selectin and von Willebrand factor [VWF]), platelets (P-selectin, glycoprotein [GP] Ibα, and high-mobility group box 1), and innate immune cells (neutrophil extracellular traps [NETs], smooth muscle cell, and monocyte-derived tissue factor) as crucial mediators of the thromboinflammatory processes underlying DVT [4–6]. This evidence concerns the gene SELP and deep vein thrombosis.