Massive studies have demonstrated that, within the tumor local inflammatory microenvironment, CDEs can transport proteins similar to parent tumor cells, proinflammatory chemokines, and cytokines, such as IL-35, IL10, TNF-α, IFN-γ, and TGF-β2, genomic DNA, mRNA, and microRNAs to interact with immune cells, including B cells, T cells, natural killer (NK) cells, regulatory T cells (Tregs), and tumor-associated macrophages (TAMs), thus weakening antitumor immune responses and escaping from immune surveillance [53, 54]. The gene discussed is TNF; the disease is neoplasm.