In NSCLC, the Cys797 mutation to serine (C797S) occurs in the EGFR moiety.3 One of the major problems of EGFR-TK is autophosphorylation, leading to signal transduction pathways that activate the ATP region of the protein due to amino acid activation in the N-lobe of the EGFR complex, leading to an unstable EGFR moiety, causing cancerous growth in the cells.4 Therefore, targeted therapy against EGFR overactivity may be effective for treating NSCLC. This evidence concerns the gene TKT and non-small cell lung carcinoma.