PFKM and neoplasm: In addition, upon C5aR1 deletion or C5aR1 inhibition in vivo, IL-22-induced AMPs led to the release of flagellin from dead bacteria, activating TLR5/AKT2 signaling pathway, which promoted PFKM stabilization and the M1 phenotype, and subsequently enhanced T cell-mediated anti-tumor immunity and suppressed CRC growth (Fig. 5G).