The major cause of drug resistance is the T790M mutation, a secondary EGFR mutation that disables TKI function and allows tumor cells to continue to rely on EGFR.[7] Recently, second-generation TKIs, afatinib, have been developed to treat lung adenocarcinoma with EGFR-activating mutations,[8] however, the response rate to T790M was not satisfactory. The gene discussed is EGFR; the disease is neoplasm.