Additionally, P.g. exploits DC-SIGN-TLR2/CXCR4 signaling, activating AKT1 and inhibiting FOXO1 by ligation via P.g. Mfa1-FimA, thereby promoting tumor-associated immunosuppression via myeloid-derived suppressor cells and Tregs [74]. The gene discussed is CXCR4; the disease is neoplasm.