The observation that miR-145 can be transferred from HMECs to U87 enforces our previous demonstration that functional gap junctions between colon carcinoma cells and HMEC could permit the transfer of miR-145-5p from cell to cell . Re-expression of miR-145 in U87 can inhibit glioma cells proliferation, invasion and angiogenesis in vitro and reduce glioma growth in vivo . This effect of miR-145 was initially related to its ability to decrease vascular endothelial growth factor (VEGF) expression levels . Actually, VEGF expression level also decreases when miR-145 expression is downregulated . Moreover, perivascular invasion by glioma cells increases when VEGF synthesis is deficient  and when brain tumor xenografts are treated with anti-VEGF blocking antibodies [24, 25]. In patients GBMs that are resistant to bevacizumab therapy, demonstrated a tendency toward perivascular invasion . Blocking angiogenic signaling using antibodies targeting the VEGF-A axis failed to curb progressive tumor growth and meaningfully extend patient survival, suggesting that both perivascular brain tumor growth and invasion use a VEGF-independent mechanism of tumor vascularization . Conversely, we here demonstrate an angiogenic effect of miR-5096, which is independent of any change in VEGF release from U87 cells. Also, overexpression and downregulation of miR-5096 did not affect the proliferation of either U87 or HMEC in vitro. Altogether, the transfer of miR via functional gap junctions between tumor cells and endothelial cells may modulate the behavior of tumor cells and surrounding normal tissues and subsequently change tumor growth characteristics [4, 6, 14].