Evidence shows its involvement at key elements of tumour growth; including tumour hypoxia triggering HIF-induced VEGF production, endogenous tumour production of VEGF, tumour-endothelium paracrine interaction and upregulation of VEGF, liberation of VEGF from the ECM by tumour heparanase production, or recruitment of VEGF producing macrophages. This evidence concerns the gene VEGFA and neoplasm.