Mechanistically, Fusobacterium nucleatum, and possibly other intestinal bacteria mediate tumor tissues’ production of inflammatory cytokines (e.g., IL-12, TGF-β, and TNF-α) (85–90), thereby affecting the heterogeneity of tumour-infiltrating Treg cells in CRCs and facilitating the expansion of pro-inflammatory FOXP3(lo) non-Treg cells that, in turn, enhances anti-tumour immunity and inhibits tumour formation (85). The gene discussed is FOXP3; the disease is neoplasm.