2006). In our study, we detected exon 19 deletion or exon 21 L858R point mutation in a NSCLC patient. These mutations increased EGFR kinase activity and resulted in hyperactivation of downstream prosurvival signaling pathways (Ladanyi and Pao 2008). In the treatment of mutated EGFR lung cancer, the first generation of tyrosine kinase inhibitors (TKIs) is commonly used, however, the efficacy of TKIs is limited due to the emergence of drug‐resistant secondary mutation T790M (Table 3), which increases ATP affinity at the ATP‐binding pocket and confers drug resistance (Yun et al. 2008). This evidence concerns the gene EGFR and non-small cell lung carcinoma.