Possible explanations could be as follows: (1) Upregulated levels of proinflammatory cytokines might trigger the expression of the serotonin transporter, elevate the reuptake of serotonin, and reduce extracellular synaptic serotonin concentrations and serotonin neurotransmission, which contributed to anxiety and depression in NSCLC survivors; thus, serum TNF‐α, IL‐1β, IL‐6, and IL‐17 were positively correlated with anxiety and depression in NSCLC survivors.10, 29. The gene discussed is IL1B; the disease is major depressive disorder.