SOAT1 and lung carcinoma: Dysfunction of cytokines and chemokines (e.g., IL‐1β, IL‐6, IL‐10, CCL2, CCL5) in TME of lung cancer were able to activate the tumor cell and inflammatory cell through signal pathway family such as nuclear factor‐kappa B (NF‐κB) family and signal transducer and activator of transcription (STAT) family which may lead to tumor immune escape, tumor angiogenesis, epithelial‐to‐transition (EMT) and anti‐apoptosis in lung cancer.42, 43, 44