MET and gastric cancer: Activation of an epithelial‐to‐mesenchymal transition (EMT) programme has been proposed as the critical mechanism for broadly regulating invasion and metastasis by epithelial cancer cells.26 EMT‐inducing transcription factors, such as snail, facilitate E‐cadherin loss, acquisition of a mesenchymal phenotype and expression of mesenchymal markers such as vimentin.27 As shown in Figure 6D, the supernatant from the macrophages treated with MET+ exosomes reduced the expression levels of E‐cadherin, while markedly increased the protein levels of vimentin and snail in GC cells.