In conjunction with the TME-induced VEGF mRNA increase in the endothelial cells shown in Fig. 1 and the reduction in Akt levels by TME shown in Fig. 3, this result suggests that although endothelial cells do increase VEGF production under TME conditions, additional paracrine stimulation from the cancer cells is important for endothelial cells to maintain Akt expression under these conditions. This evidence concerns the gene AKT1 and cancer.