In contrast, CLEC-2 has been shown to drive thrombosis at sites of inflammation in the venous system in mouse thrombo-inflammatory models, namely DVT and bacterial infection.252Platelet activation in these models is mediated by inflammation-driven up-regulation of the ligand for CLEC-2 in the vessel wall podoplanin. The gene discussed is CLEC1B; the disease is deep vein thrombosis.