In the context of the TME, Tregs are highly effective at dampening anti-tumor immunity through several mechanisms, including the following: the expression of constitutively high levels of the immune checkpoint molecules CTLA-4 and PD-1, release of immune suppressive cytokines such as interleukin (IL)-10 and transforming growth factor (TGF)-β, metabolic consumption of IL-2 through expression of the high affinity chain of the IL-2R (CD25), and direct killing of effector CD8+ T cells [4]. The gene discussed is TGFB1; the disease is neoplasm.