Overall, our findings indicated that LukS-PV targeting C5aR1 downregulated HDAC7 to upregulate the acetylation level of β-catenin, thus promoted its protein degradation and reduced entry into the nucleus, led to target gene transcription inactivated, and ultimately inhibited HCC cell proliferation (Fig. 9). The gene discussed is HDAC7; the disease is hepatocellular carcinoma.