Anti-Pdpn antibody treatment and CLEC-2 deletion resulted in a reduction of thrombus formation. Pdpn overexpression was strongly associated with the amount of intratumoral thrombotic vessels and increased VTE risk in cancer patients. Anti-Pdpn antibody treatment inhibited platelet activation in vitro and decreased the incidence of VTE in mice. The gene discussed is PDPN; the disease is cancer.