The inhibitors targeting TKD of EGFR have been approved in non-small cell lung cancer; however, these EGFR tyrosine kinase inhibitors (TKIs) are especially more active in constitutively active mutant EGFRs, most notably exon19-deletion and exon 21-L858R, than in wild-type (WT) EGFR [13–17]. This evidence concerns the gene EGFR and non-small cell lung carcinoma.