EGFR mutations serve as a pivotal driver in NSCLC, where their aberrant activation promotes tumor proliferation, metastasis, and survival through downstream signaling pathways. Although EGFR-TKIs effectively target mutant EGFR, acquired resistance significantly diminishes their clinical efficacy. Recent studies have demonstrated that ncRNAs play a critical role in the dynamic regulatory network of the EGFR signaling pathway and are deeply implicated in the development of EGFR-TKI resistance in lung cancer. This review focuses on the dynamic bidirectional regulatory mechanisms between ncRNAs and the EGFR signaling pathway, as well as the multifaceted molecular mechanisms through which ncRNAs mediate resistance to EGFR-TKI therapy. Elucidating the interaction network between ncRNAs and the EGFR pathway not only provides novel molecular insights into resistance mechanisms but also establishes a theoretical foundation for developing ncRNA-based combination therapeutic strategies and dynamic biomarkers for monitoring resistance evolution, highlighting significant translational and clinical potential.