Pharmacologically the proof was such that it was based on the inhibition of the angiogenesis using molecular and biochemical methods like targeting bFGF using an anti bFGF antibody was synthesized in the laboratory and then introduced to mice bearing the tumour, resulted in dramatic reduction in neovascularization as well as the tumour volume. Showed that if neovascularization is not there then tumour growth can be stopped. This showed that if neovascularization is not there then tumour growth can be stopped. Biological evidence was also generated and that evidence based on the condition of the cell culture like Human retinoblastoma that has metastasized to the vitreous is viable and a vascular and tumour spread is restricted. (Folkman, 2001) means that since it is a vascular treatment and it does not have its own blood supply it can only maintain it’s life if it is getting blood from the nearby vessels which will not give it enough capability to increase in size and gets metastasized. Genetic evidence is the most convincing and direct one. Genetically the evidence was based on the transfection of genes for antiangiogenic proteins into cancer cells such as the down-regulation of the ras oncogene in a melanoma, resulted to huge cell death of microvascular endothelium in the tumour mass starting within 6 hours. Tumour cells commence to die days later and the tumour mass had totally disappeared by 12 days. The tumour angiogenesis or Neovascularisation of tumour tissue is considered as the fundamental mechanism for the tumour growth, proliferation not only the growth of the tumour but also the tumour invasion and metastasis become angiogenesis-dependent, and this appears to be an essential process at the beginning as well as at the end of the metastatic cascade. .