BMSCs exhibit dual regulatory roles in lung adenocarcinoma (21), dynamically influencing tumor progression through CXCR4-mediated homing to the microenvironment where they secrete pro-angiogenic (VEGF), pro-metastatic (IL-6, TGF-β), and immunosuppressive factors, while paradoxically suppressing metastasis via TRAIL-induced apoptosis or differentiation into cancer-associated fibroblasts under specific conditions, with these opposing effects governed by BMSC heterogeneity and inflammatory signaling dynamics within the tumor niche (22). This evidence concerns the gene TGFB1 and neoplasm.