Additionally, an abnormally active lipid metabolism pathway in smoking‐associated specific TNFRSF9hiADAM12+CD4+ Tregs, which serve as the energy source for the transition of cytotoxic T lymphocyte‐associated antigen‐4 (CTLA‐4)+ Tregs into exhausted cells induced by the interaction of ADAM12–ITGB1, was found in a study of T‐cell development trajectories in patients who smoke and have non‐small cell lung cancer, and this high lipid metabolism rate is closely associated with enhanced fatty acid synthesis in terminal ADAM12+CTLA‐4+CD4+ Tregs.123. This evidence concerns the gene CD4 and lung cancer.