,77 This shift toward a higher population of Tregs in the TME is largely driven by signaling molecules, including TGF-β, IL-10 and miR-155, which are packaged into exosomes and delivered to CD4+ T cells.78, 79, 80 The expansion of Treg further contributes to immune suppression by inhibiting the function of other immune cells, promoting tumor cell survival, and dampening anti-tumor immunity.81 Here, TGFB1 is linked to neoplasm.