Exhausted T cells are constantly stimulated by chronic inflammatory pathogens or tumor antigens and gradually lose their abilities of antigen recognition, proliferation and activation, secretion of interleukin-2 (IL-2) and tumor necrosis factor α (TNF-α), or completely lose their abilities to produce interferon-γ (IFN-γ), chemokines, and degranulation, which finally leads to the stepwise loss of effector functions and impaired elimination of viral or tumor antigens [6, 7]. This evidence concerns the gene IL2 and neoplasm.