Background: The role of EGFR tyrosine kinase inhibitors (TKIs) as adjuvant therapy in EGFR-mutated NSCLC is still controversial. Identifying biomarkers associated with increased risk of recurrence may help stratify pts & guide adjuvant therapy. We hypothesized that tumor immune microenvironment (TME) alterations could predict disease-free survival (DFS) in these pts. Methods: The Cancer Genome Atlas (TCGA) lung Adenocarcinoma (LUAD) data at Genomic Data Common (GDC) was accessed for pt phenotype, updated outcome & normalized gene expression profile (RNA seq). Immune landscape data was obtained from PANCAN. We chose to focus on 54 key TME genes, identified from a commercially available immune report card from OmniSeq (Inc.). Pt groups were divided via K-mean clustering. Group comparison was done via Likelihood Ratio (LR, categorical), Mann Whitney (continuous), log-rank (survival) & Cox regression (outcome). Bonferroni correction was used to correct for multiple comparisons. Results: 877 pts with LUAD were identified, 32 of whom had EGFR mutations and were at stages I to III. The mutations were mostly in the TK domain, involving exons 18 (12%), 19 (27%), 20 (6%), & 21 (33%). Only 3% harbored the T790M mutation. None of the pts received adjuvant TKI. Analysis of the impact of individual genes on DFS yielded a group of 8 genes whose high expression was associated with improved DFS: IL10 (HR 0.58, p 0.029), BTLA (HR 0.66, p 0.07), CD8A (HR 0.6252, p 0.099), CD39 (HR 0.454, p 0.037), CCR2 (HR 0.729, p 0.039), CSF1R (HR 0.70, p 0.087), ICOS (HR 0.66, p 0.062), & CD4 (HR 0.67, p 0.059). K-mean clustering of the pts using these genes demonstrated 2 groups with distinct immune profiles. Group 1 was characterized by higher leukocyte and stromal fractions, lymphocyte infiltration score, macrophage regulation, TGF-ß response, & T cell richness with less proliferation, pointing towards a more “inflamed” phenotype. Significant difference between the two groups in the immune subtypes was found (LR 10, p = 0.039). 90% of pts in the inflamed group had tumors with IFN-γ dominant, inflammatory, and TGF-ß dominant subtypes, while 45% of the “non-inflamed” group had lymphocyte depleted & wound healing signatures. DFS was significantly longer in the inflamed group (median DFS 1480 vs 772 days, p = 0.002). Conclusions: In pts with resected EGFR-mutated LUAD, an inflamed TME is associated with prolonged DFS. Identifying these pts may help select those who would benefit from adjuvant therapy.