The discovery of HIF-1, and the identification of VEGF as one of its transcriptional targets (Maxwell et al., 1997), ultimately allowed building the current model for tumor angiogenesis: (i) A massive cell growth in a tumor rapidly provokes hypoxia, (ii) HIF induces the expression of VEGF by tumor cells, and (iii) VEGF is the angiogenic signal that allows the recruitment of new blood vessels by the tumor. This evidence concerns the gene HIF1A and neoplasm.