Senescent T cells can regulate the tumor microenvironment and perform intercellular communication through the senescence-associated secretory phenotype (SASP) and maintain metabolic activity, producing substantial amounts of inflammatory cytokines such as interleukin-2(IL-2), IL-6, IL-8, tumor necrosis factor (TNF), and interferon-gamma (IFN-γ), as well as inhibitory cytokines such as IL-10 and transforming growth factor beta (TGF-β) [19,20]. The gene discussed is TNF; the disease is neoplasm.