More recently, in a mouse model of either spontaneous or experimentally induced lung metastasis, obtained by injection of Lewis lung carcinoma (LLC) cells and B16 melanoma cells respectively, P2Y12 deficiency reduced the weight of lung metastasis without affecting the primary tumors (Wang et al., 2013). This suggests a role for the ADP receptor in promoting the metastatic process. This hypothesis was strengthened by the observation that platelets from P2Y12-deficient mice significantly reduced the invasiveness of LLC cells. Moreover, P2Y12 deficiency reduced the capability of the cancer cells to stimulate the production of active TGFβ1 from platelets. This, in turn, resulted in the prevention of platelet-induced epithelial-mesenchymal transition (EMT) of the tumor cells (Wang et al., 2013), a process known to contribute pathologically to cancer progression and metastasis.