Furthermore, EVE, in combination with somatostatin analogs, demonstrated a synergistic anti-angiogenic effect, whereby EVE reduced the production of VEGF by tumor cells by inhibiting the mTOR-HIF-1α pathway, while somatostatin analogs acted directly or indirectly on stromal endothelial cells and monocytes expressing somatostatin receptors (123). This evidence concerns the gene MTOR and neoplasm.