Abstract
The resistance mechanisms to EGFR-TKIs are inevitable and heterogeneous. Secondary T790M mutation was the most frequent acquired resistance mechanism to early-generation EGFR-TKIs and osimertinib was the standard second-line therapy. Driver gene alterations like ALK and MET were increasingly observed in resistance mechanisms. Additionally, driver gene resistance overlaps with EGFR T790M accounted for 4%-8% in resistant patients. However, no good consensus was formulated.
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