Gastric cancer (GC) is the third most important cause of global cancer mortality.1 Although improved treatment, such as surgery and chemotherapy, has been effective in reducing mortality, the 5-year survival rate of GC patients remain relatively low.2 Increasing studies have reported that metastasis is responsible for GC-related deaths by the dysregulation of multiple genes, including p53, c-met and k-ras.3 However, the mechanisms of cell differentiation, proliferation and metastasis remain largely unknown. This evidence concerns the gene KRAS and gastric cancer.