For instance, EVs derived from breast cancer cells had an upregulated display of VEGF which stimulated the VEGFR‐signaling within the endothelial cells, with enhanced total VEGF secretion under hypoxic conditions promoting angiogenesis [81], or breast cancer cells derived EVs promoted epithelial to mesenchymal transition (EMT) by stimulating TGF‐β signaling due to the transfer of TGF‐beta II receptor, which is expressed on the EVs, promoting cancer stemness, metastasis and CD8+ T cells exhaustion by breast cancer cells [82]. This evidence concerns the gene VEGFA and cancer.