(i) Senescent T cells have unique phenotypes with impaired antitumor activities. They downregulate the costimulatory molecules CD27 and CD28 as well as the effector molecules perforin and granzyme, and decrease proliferation, but promote cell cycle arrest and expression of molecules that inhibit proliferation. (ii) Senescent T cells can actively influence other immune cells within the tumor microenvironment. In addition to inducing adaptive Tregs, they can become potent suppressor cells themselves, performing direct inhibition on DCs and effector T cells. (iii) Senescent T cells have a unique SASP, secreting large amounts of cytokines that can induce premature senescence in T cells (IL-6, IL-8, TNF) and suppress effector immune cells (IL-10, TGF-β), as well as disrupt normal mammary differentiation and promote malignant phenotypes and tumor cell growth. (iv) Senescent T cells with potent suppressive activity can directly suppress effector T cell proliferation and function. (v) Senescent T cells can promote tumor growth, invasion, metastasis, and epithelial-to-mesenchyme transition via SASP or cell-cell direct contact.