HDAC7 and hepatocellular carcinoma: In this study, we found that bacterial toxin LukS-PV targeting complement receptor C5aR1 downregulated HDAC7 expression to upregulate the acetylation level of β-catenin, thus promoting the degradation of β-catenin and reducing entry into the nucleus, led to target gene transcription inactivation, and ultimately inhibited HCC cell proliferation.