There is evidence in the literature that CLEC-2 plays a role in thrombosis and hemostasis, probably in conjunction with glycoprotein VI (GPVI) as deletion of both CLEC-2 and GPVI in mice causes bleeding and reduced arterial thrombus formation.12Furthermore, CLEC-2 is known to promote hematogenous tumor metastasis of podoplanin-expressing cells.13Finally, high podoplanin expression in primary brain tumors is associated with an increased risk of venous thromboembolism, due to platelet activation via the CLEC-2/podoplanin interaction.14 This evidence concerns the gene CLEC1B and venous thromboembolism.