In lung cancer, Tregs suppress antitumor CD4+ and CD8+ T‐cell responses, contributing to disease progression.11 Antigen recognition in the presence of transforming growth factor β (TGFβ) and IL‐10, which are produced within the lung tumor environment, induces CD4+ T‐cell differentiation into inducible Tregs (iTregs).13, 14 Once activated, Tregs can then exert their immunosuppressive function on effector CD4+ and CD8+ T cells, namely through further secretion of inhibitory cytokines, including TGFβ, IL‐10 and IL‐35.11 This evidence concerns the gene CD8A and lung cancer.