Several features of Tregs, such as the increased production of suppressive cytokines (TGF-β, IL-10, IL-35), upregulation of immune checkpoints and inhibitory receptors (CTLA-4, PD-1, LAG-3, TIM-3, ICOS, TIGIT, IDO), direct cytotoxicity (perforin/granzyme-mediated), disturbance of T effector cell activity (IL-2 consumption), and induction of tolerogenic DCs, support tumor cell growth and create a niche that provides resistance to conventional chemotherapy and even immunotherapy [34]. The gene discussed is PRF1; the disease is neoplasm.