However, the over-expression of endogenous inhibitors like tumstatin, but also endostatin or thrombospondin-1 (TSP-1), induces the upregulation of angiopoietin-2, basic fibroblast growth factor (bFGF) and platelet-derived growth factor type A (PDGF-A) in colon cancer cells as a mechanism of escape from anti-angiogenic stimuli [61], and the use of these fragments is more effective when used in combination with other angiogenic inhibitors or conventional chemotherapy/radiotherapy. This evidence concerns the gene COL4A3 and colonic neoplasm.