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 TNFSF10 and lung adenocarcinoma.