It has been hypothesized that exposure of vWF on the activated endothelial cell surface could also support the recruitment of platelet-cancer cell aggregates since genetic deficiency or antibody-mediated blockade of GPIbα, a vWF binding receptor on the platelet surface could inhibit TCIPA, also platelet-tumor cell interactions with endothelial cells, and consequent lung metastasis (128, 129). Here, GP1BA is linked to neoplasm.