Abstract
Intervention using molecular targeted agents for non-small cell lung cancer (NSCLC) with driver oncogenes has facilitated tumor evolution, leading to acquired drug resistance. However, clinical studies have demonstrated limited outcomes for NSCLC patients with acquired resistance. The maintenance of residual tumor cells during treatment may be accelerated by various molecular mechanisms and eventually enhances tumor recurrence. Currently, drug tolerant (DT) cells play a pivotal role in the progression of tumor heterogeneity.
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