Collectively, these findings derived from integrative bioinformatics, protein-level validation in EGFR-mutant tumors, and matched resistant tumor biopsies, suggest that LAPTM4B is a clinically relevant factor in EGFR-mutant NSCLC and may contribute to the molecular underpinnings of acquired resistance to EGFR-targeted therapy. The gene discussed is EGFR; the disease is neoplasm.