One of the mechanisms of EGFR‐TKIs resistance is the binding of hepatocyte growth factor (HGF) ligands and c‐Met, which could activate c‐Met, inducing homodimerization and phosphorylation of intracellular tyrosine residues, eventually promoting tumor immune escape by activating the PI3K/AKT and MAPK signaling pathways and inducing the upregulation of PD‐L1 through activator protein‐1 (AP‐1). The gene discussed is AKT1; the disease is neoplasm.