Cellular senescence orchestrates immune evasion and chronic inflammation in lung cancer through SASP-mediated immunosuppression and mitochondrial dysfunction (28).SASP-derived pro-inflammatory cytokines (IL-6, IL-8, TNF-α) and chemokines (CCL2, CXCL1) directly suppress antitumor immunity: IL-6 activates JAK/STAT3 signaling to upregulate PD-L1 expression on tumor cells and dendritic cells, inducing CD8+ T cell exhaustion (77). The gene discussed is CCL2; the disease is neoplasm.