The promising effect of this combination on delaying or preventing the emergence of acquired resistance is largely due to its effectiveness in eliminating both primarily resistant clones and DTCs present in the EGFRm NSCLC cell population, which both constitute a key mechanism accounting for the emergence of acquired resistance to EGFR-TKIs, including osimertinib (18, 19). This evidence concerns the gene EGFR and non-small cell lung carcinoma.