Mice with a deficiency in CLEC-2 are protected against deep vein thrombosis [11], and CLEC-2 activation by podoplanin plays a role in inflammation-driven murine hepatic thrombosis [56], and possibly in human venous thrombosis [12] whilst it is apparently not involved in primary hemostasis [55]. This evidence concerns the gene CLEC1B and deep vein thrombosis.