c‐Met is phosphorylated and subsequently activates motility, proliferation, invasion, and migration.18 Previous studies found that inhibition of c‐Met phosphorylation and its downstream cascade, such as suppression Akt phosphorylation and mammalian target of rapamycin (mTOR) phosphorylation, might provide new therapeutic strategies for various cancers.16, 19 Our study suggests that MACC1 regulates PDL1 expression via the c‐Met/AKT/mTOR pathway in GC cells. Here, MET is linked to gastric cancer.