EGFR tyrosine kinase inhibitors (TKI), such as gefitinib, erlotinib or afatinib, preferentially target lung tumors with mutated-EGFRs, but not the wild-type EGFR (WT-EGFR) tumors, suggesting that the mutated- and WT-EGFRs have different oncogenic effects. EGFR protein expression was previously detected in various solid tumors, and EGFR expression correlated with cell migration/invasion in breast and oral cancer cell lines [11–13]. However, the ability of EGFR to enhance cell motility is ligand-dependent [11–13]. The participation of activating EGFR mutations in lung cancer cell mobility is unknown.