At progression, the emergence of additional mutations is implicated in resistance to therapy and tumor progression.29,35,40 The molecular mechanisms of acquired resistance with mefatinib were predominantly EGFR T790M, consistent with other commercially available first- and second-generation EGFR-TKI.6,14,15,40,41 Other common bypass mechanisms, including MET and ERBB2 amplifications, were also identified in our cohort. This evidence concerns the gene EGFR and neoplasm.