A molecular marker that can predict efficacy is the mutational status of the epidermal growth factor receptor (EGFR) gene, whose exon 19 and 21 mutations are used to predict EGFR-tyrosine kinase inhibitor (TKI) efficacy. The objective efficiency of first-line treatment with chemotherapy is about 40%-50%, and only about 30% if EGFR-TKI (hereafter referred to as TKI) is applied directly to first-line treatment without selection. the results of the IPASS study showed that TKI was more effective than chemotherapy for EGFR mutation-positive patients, while TKI was also less effective than chemotherapy for EGFR wild-type patients DD If patients were EGFR mutation-positive, then TKI first-line treatment can be chosen, and if mutation-negative, then first-line chemotherapy should be chosen. The significance of testing EGFR at second and third line treatment is to find the superior population. Since the efficiency of second- and third-line chemotherapy is only about 10%, and the results of the INTEREST study suggest that TKI efficacy is comparable to chemotherapy. What is known is that in second- and third-line therapy, EGFR mutation-positive individuals have a greater chance of benefiting from TKI therapy than wild-type patients, and the purpose of EGFR testing at second- and third-line therapy is actually to screen for a superior population. The purpose of EGFR testing in second and third-line therapy is to screen for the superior population, which is of great significance to clinicians in choosing “early” or “late” TKI treatment. The earlier positive patients are screened and treated, the greater the potential benefit. It should be noted, however, that it is not true that TKI cannot be used in EGFR wild-type patients, for whom chemotherapy is available in the second line, but there is no standard treatment in the third line. Some studies have shown that wild-type patients can still benefit from TKI therapy compared to placebo.