For instance, the gastric cancer cells treated with HGF (−)/c‐met (+) were accompanied with increased expressions of Snail‐2, E‐cadherin vimentin and other EMT‐relevant proteins, and cells assumed such changes as loss of polarity and increased pseudopodium of mesenchymal cells.52 Furthermore, c‐met also mediated epithelial‐mesenchymal transition (EMT) of breast cancer cells via activation of c‐Src and Stat3.53 This evidence concerns the gene HGF and breast carcinoma.