Our findings demonstrate that inhibiting FAK is an effective means of sensitizing EGFR wild-type NSCLC cell lines to EGFR TKIs and that FAK inhibitors used in combination with erlotinib may be more effective than treatment with erlotinib alone in inhibiting EGFR TKI-resistant NSCLC cell viability and tumor growth. This evidence concerns the gene EGFR and neoplasm.