The TME is populated by regulatory T-cells (Tregs), myeloid-derived suppressor cells (DSCs), and tumor-associated macrophages (TAMs) with an M2 phenotype, that collectively switch off anti-tumor effects by producing immunosuppressive factors such as transforming growth factor-beta (TGF-β) and interleukin-10 (IL-10) [91]. The gene discussed is TGFB1; the disease is neoplasm.