Recent studies in KRAS-mutant lung cancer (54, 55) and pancreatic adenocarcinoma (55), KRAS-amplified gastric carcinoma (56), and multiple other cancer models expressing mutant or wild-type KRAS (57, 58) revealed that the anti-tumor effect of MEK inhibitor treatment could be dramatically potentiated by concurrent SHP2 inhibition. This evidence concerns the gene KRAS and gastric carcinoma.