(2) Tissue destruction by surgical resection might induce the release of damage‐associated molecular patterns in response to treatment‐associated cell death, which activated the expression of the transcription factor nuclear factor‐κ‐β and exaggerated the production of proinflammatory cytokines, thereby contributing to increased serum TNF‐α, IL‐1β, and IL‐17 levels in NSCLC survivors compared with controls.26 The gene discussed is IL1B; the disease is non-small cell lung carcinoma.