Interestingly, P.g. appears to exploit two distinct fimbrial pathways: Mfa1-DC-SIGN, which promotes immunosuppression via pAKT1–pFOXO1–STAT3–IDO1–FOXP3 leading to Treg activation and myeloid-derived suppressor cell differentiation, and FimA that activates oncogenes such as CXCR4 and SDF-1, and silences tumor suppressors like LDOC1 and FOXO3 [74]. The gene discussed is FOXO3; the disease is neoplasm.