c‐Met activation of a variety of tumor cell types plays an important role in regulating tumor progression,11 and c‐Met/AKT/mTOR pathway is involved in hepatocyte growth factor (HGF)‐promoted epithelial‐mesenchymal transition (EMT) and angiogenesis.12 To investigate the role of the c‐Met/AKT/mTOR pathway in c‐Met‐mediated PDL1 expression, we used SU11274, MK2206, and rapamycin to inhibit the c‐Met/AKT/mTOR pathway. The gene discussed is AKT1; the disease is neoplasm.