H2AZ1 and neoplasm: Taken together, in the present study, we showed that H2A.Z.1 is up-regulated in HCCs and that targeted inactivation of H2A.Z.1 inhibits in vitro liver tumorigenesis by selectively modulating cell cycle and EMT regulatory proteins in liver cancer cells, which suggested that the development of specific H2A.Z.1 modulators may be crucial for helping to control tumor progression or even for reversing cancer phenotype.