Hence, in the present work, we proposed to target the mTOR pathway with Everolimus (E) and simultaneously disrupt the VEGF-NRP1 axis by using EG00229 (G) that might block both VEGF/VEGFR2/NRP1-mediated proangiogenic signaling pathways in endothelial cells and VEGF/NRP1/Ras-mediated autocrine activation of tumor cell growth.16 We assumed that by doing so, our strategy will reduce the amount of available VEGF and, at the same time, inactivate the residual VEGF from activating its proangiogenic and pro-tumorigenic downstream signaling pathways. This evidence concerns the gene MTOR and neoplasm.