A comparison of PC3 intravasation variants pointed to key roles for the uPA-plasmin system, possibly via promoting tumor cell matrix invasion and facilitating the development of VEGF-dependent angiogenic blood vessels [110]; thus, inhibition of pro-uPA activation, at the apex of the uPA/plasmin cascade, could be an approach to control the onset of tumor escape and metastatic spread [111]. This evidence concerns the gene VEGFA and neoplasm.