Further in vitro experiments have shown that hepatocyte growth factor (HGF) is effectively activated by such translocated EGFR by the suppression of miR-26a/b, and the upregulated paracrine HGF, which binds the c-MET receptor onto migrated cancer cells, establishes a fertile microenvironment so that metastatic gastric cancer cells can land and proliferate. This evidence concerns the gene EGFR and gastric cancer.