GSEA unraveled that spliceosome, nucleotide excision repair, DNA replication, cell cycle, homologous recombination, ubiquitin mediated proteolysis, mismatch repair, p53 signaling pathway, oocyte meiosis and pyrimidine metabolism were significantly enriched in the high CENPL expression phenotype (Table 4; Figure 5A), indicating that elevated CENPL might participate in the occurrence and progression of HCC through these pathways. Here, TP53 is linked to hepatocellular carcinoma.