In the context of NSCLC, tumor-derived EVs can accelerate angiogenesis and tumor growth in a TGFβ1-dependent pathway23 by enhancing VEGF levels via miR-21 transfer24, by TIMP-1-induced miR-210 transfer25, as well as by miR-23a transfer under hypoxic conditions26. The gene discussed is VEGFA; the disease is neoplasm.