found that in HBV-related HCC cells, HBX not only suppressed the expression of AIM2 at the gene level by promoting the stability of the enhancer of zeste homolog 2 (EZH2), but also interacted with AIM2, resulting in AIM2 degradation via the ubiquitin-proteasome pathway. This evidence concerns the gene AIM2 and hepatocellular carcinoma.