The highly coordinated mechanisms of action of PGs in cancer depend on direct interactions with cell surface receptor tyrosine kinases (RTKs), such as MET and vascular endothelial growth factor receptor 2 (VEGFR2), integrins, and Toll-like receptors that are expressed by stromal cells, breast cancer cells, and macrophages [20,26,27,28]. The gene discussed is MET; the disease is breast cancer.