In fact, evidence suggests that PDPN and CLEC-2 play a mechanistic role in the process of thrombus formation both in an inferior vena cava stenosis mouse model of DVT, where both inhibition of PDPN as well as CLEC-2 deficiency resulted in significantly reduced extension of thrombosis, and in an in vivo mouse model of infection-driven thrombosis.80 In patients with brain tumours, PDPN overexpression is strongly correlated with the presence of intratumoural thrombotic vessels, hypercoagulability and increased VTE risk. This evidence concerns the gene CLEC1B and brain neoplasm.