In summary, the current findings suggest that CXCR1+ neutrophil infiltration in pretreatment tumor tissues was associated with the efficacy of third-generation EGFR-TKI and increased CXCR1+ neutrophil infiltration in posttreatment tumor tissues played a role in mediating the resistance to third-generation EGFR-TKI in EGFR-mutant NSCLC patients, underscoring the clinical significance of CXCR1+ neutrophils within the tumor microenvironment. The gene discussed is CXCR1; the disease is neoplasm.