However, it has recently been reported that combined in vivo depletion of the collagen receptor glycoprotein (GP) VI and CLEC-2 severely compromises hemostasis and abrogates arterial thrombosis in mice[11], indicating that CLEC-2 plays a role in thrombosis and hemostasis, although deletion of CLEC-2 alone produces a relatively minor phenotype. The gene discussed is CLEC1B; the disease is Venous thrombosis.