In LUAD, the tumor microenvironment (TME) is orchestrated by immunosuppressive niches dominated by (a) dysfunctional T cell populations with exhausted phenotypes, (b) M2-polarized tumor-associated macrophages (TAMs) promoting immune evasion, (c) PD-1/PD-L1-driven myeloid suppression, and (d) cancer-associated fibroblasts (CAFs) that drive metastatic progression through TGF-β/IL-6-mediated ECM remodeling and angiogenic reprogramming.14,20. The gene discussed is TGFB1; the disease is neoplasm.