HBx was shown to interact with HDAC1 and HDAC2, and HBx-induced stabilization of hypoxia-inducible factor 1 alpha (HIF-1α), a key regulator in tumor growth, angiogenesis and metastasis of HCC, involved deacetylation by HDAC1 [191,229]. This evidence concerns the gene HDAC2 and neoplasm.