Previous studies suggested that CDCA8 interacted with Survivin to positively regulate the segregated chromatids and abnormal mitotic bridges.[24] Moreover, disruption of the interaction between CDCA8 and Survivin inhibited the growth of hepatocellular carcinoma.[28] A functional CPC required aurora B activity and INCENP, Survivin and CDCA8 for proper activation and localization of the kinase. This evidence concerns the gene AURKB and hepatocellular carcinoma.