Majority of the NSCLC patients worldwide are EGFR wild type.34 However, numerous receptor tyrosine kinase inhibitors target mutation‐positive NSCLC35, 36 and wild type EGFR patients lack effective treatments that significantly improve their survival and prognosis.13, 34 In this study, DUXAP9‐206 was found to inhibit the degradation of EGFR in EGFR wild type NSCLC cells, such as A549 and H1703, indicating that DUXAP9‐206 may be a promising therapeutic target for EGFR wild type patients in NSCLC. This evidence concerns the gene DUXAP9 and non-small cell lung carcinoma.