The following were possible explanations: (1) Dysregulated immune host cells (such as infiltrated inflammatory cells and endothelial cells) after surgery produced high levels of proinflammatory cytokines in the tumor microenvironment; thereby, NSCLC survivors had higher serum TNF‐α, IL‐1β, and IL‐17 levels than controls.25 The gene discussed is IL1B; the disease is neoplasm.