In the presence of endothelium-derived Gas6, tumor cells induce phosphorylation of Erk1/2 in endothelial cells, leading to an upregulation of Ptges production. Ptges produces PGE₂ from prostaglandin H₂ (PGH₂), which, on secretion, interacts with the EP3 receptor on platelets to trigger platelet activation and promote thrombosis. Whether the effects mediated by Gas6 are due to an interaction of Gas6 with the tumor cell or through an autocrine signaling in the endothelial cell is still unknown.