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Somatic mutations in the epidermal growth factor receptor ( EGFR ) gene are present in approximately 20% (in Caucasians) to 40% (in East Asians) of adenocarcinomas of the lung. Targeted therapy for these lung cancers has been established based on evidence regarding mainly common mutations; that is, exon 19 deletions (Del19) and L858R.  EGFR ‐tyrosine kinase inhibitors ( TKI ), gefitinib, erlotinib or afatinib showed high objective response rates ( ORR ) of approximately 60%. Several studies suggested that Del19 might be more sensitive to  EGFR ‐ TKI  than L858R. On the other hand, it has been difficult to establish evidence for other less common mutations, accounting for 12% of all  EGFR  mutations, because there are many variants and many studies have excluded patients with these uncommon mutations. However, recent studies revealed that these rare genotypes could be targetable if appropriate  TKI  are selected. For example, G719X (X denotes A, S, C and so on), Del18, E709K, insertions in exon 19 (Ins19), S768I or L861Q showed moderate sensitivities to gefitinib or erlotinb with  ORR  of 30%–50%. However, afatinib appeared to be especially effective for these tumors. Although Ins20s (except for ins FQEA ) have been regarded as resistant mutations, osimertinib may be effective for rare subtypes of them and nazartinib ( EGF 816) is promising for the majority of them. For the further development of targeted therapy in all  EGFR  mutations, it is important to precisely detect targetable mutations, to select the most appropriate  TKI  for each mutation, and to continue investigating  in vitro  studies and collecting clinical data on even rare mutations.

Not all epidermal growth factor receptor mutations in lung cancer are created equal: Perspectives for individualized treatment strategy