In contrast, pharmacological inhibition of C5aR1 signaling by its antagonist PMX-205 or deletion of C5aR1 is sufficient to attenuate the immunosuppressive microenvironment, suppress tumor growth, and reduce lung metastases [10, 11], highlighting the potential value of targeting C5aR1 for CRC treatment. The gene discussed is C5AR1; the disease is neoplasm.