In our work, we also showed that the proportion of patients with RB1 mutations in CDCA5-high group was statistically higher than that in CDCA5-low group, suggesting that inactivation of pRB can lead to abnormally up-regulation of CDCA5 during carcinogenesis, which contribute to HCC tumor cell proliferation. This evidence concerns the gene RB1 and hepatocellular carcinoma.