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    The treatment landscape of epidermal growth factor receptor (EGFR)–mutant advanced NSCLC has rapidly evolved. Third-generation tyrosine kinase inhibitors (TKIs) are now the preferred standard treatment option in the first-line setting 1 on the b asis of prolonged progression-free survival (PFS) and superior intracranial activity when compared with first-generation epidermal growth factor receptor (EGFR) TKIs. 2 – 7 Unfortunately, resistance inevitably develops. Although several mechanisms of acquired

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