Tumours achieve these differences largely through an up-regulation of pro-angiogenic factors such as vascular endothelial growth factor (VEGF) and tumour growth factor-β (TGF-β) and a down-regulation of anti angiogenic factors such as Thrombospondin-1 (TSP-1), causing the ‘angiogenic switch’ to be permanently switched to ‘on’ [32–35]. This evidence concerns the gene VEGFA and neoplasm.