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Figure 2. Integrative analysis of tumor heterogeneity and emerging technologies in lung cancer immunotherapy. This concentric illustration highlights the multi-dimensional heterogeneity of the TME, emphasizing molecular, cellular, and spatial complexity in lung cancer. Molecular heterogeneity, driven by genetic mutations (e.g., EGFR, KRAS) and epigenetic alterations activating oncogenic pathways such as RAS-MEK signaling, forms the core of tumor progression and immune evasion. Cellular heterogeneity emerges through complex interactions among immune and stromal cell subsets - including Tregs, NK cells, CTLs, MDSCs, TAMs, CAFs, and NETs - facilitating immunosuppression. At the outer layer, spatial heterogeneity reflects cell organization into immune-active hotspots and immunologically cold zones shaped by physical barriers, such as the ECM. Advanced technologies, including spatial omics, single-cell sequencing, liquid biopsy, organoids, AI analytics, and nanotechnology, enable precise characterization and therapeutic targeting of these heterogeneities. TME: Tumor microenvironment; EGFR: epidermal growth factor receptor; KRAS: Kirsten rat sarcoma viral oncogene homolog; RAS-MEK: RAS- mitogen-activated protein kinase kinase; Tregs: regulatory T cells; NK cells: natural killer cells; CTLs: cytotoxic T lymphocytes; MDSCs: myeloid-derived suppressor cells; TAMs: tumor-associated macrophages; CAFs: cancer-associated fibroblasts; ECM: extracellular matrix; NETs: neutrophil extracellular traps.