CLEC1B and infection: 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.