Such patients can develop progressing lesions at multiple metastatic sites, and each of the metastases in a patient can have different genomic mutational resistance mechanisms.10–12 Furthermore, sensitivity to TKIs varies considerably depending on the type of secondary mutation.7,13 One of the mechanisms of acquired resistance to EGFR-targeted inhibitors in EGFR-mutated lung cancer is the occurrence of a secondary mutation (T790M, C797S) in the kinase domain.14 Therefore, it is essential to validate novel therapeutic strategies. This evidence concerns the gene EGFR and lung carcinoma.