A comparison was made between tumors derived from 786-O cells expressing VHL with inactivated HIF1α degradation and tumors derived from 786-O cells expressing VHL with intact HIF1α degradation but inactivated collagen/fibronectin interaction; it indicated that the elevation of the angiogenic growth factor VEGF by stabilized HIF1α is not sufficient to generate the highly vascular tumor phenotype. This evidence concerns the gene HIF1A and neoplasm.