The results revealed that the microbial metabolite, short-chain fatty acid, triggered a sequence of antitumor immune responses by binding to G protein-coupled receptor 43 (GPR43) in the gut, including significantly increasing the levels of infiltrating CD8+, IFN-γ+ CD8+ and CD4+ T cells within tumor tissues, instigating dendritic cell maturation, facilitating the polarization of tumor-associated M2 macrophages into pro-inflammatory M1 macrophages, and diminishing the occurrence of immunosuppressive myeloid-derived suppressor cells (MDSCs) [10]. The gene discussed is CD4; the disease is neoplasm.