In addition, anti-C5aR1 Ab reduced PFKM ubiquitination in peritoneal macrophages from tumor-bearing mice (Fig. 2L), suggesting that upon C5aR1 inhibition or C5aR1 deletion, PFKM stabilization mediated by AKT2 activation was required for the M1 phenotype. Here, AKT2 is linked to neoplasm.