Overexpression of RPL8 enhances cell growth, mobility, and glycolytic activity in HCC.38 SUV39H1, a methyltransferase, utilizes SAM to drive H3K9me3 modification, suppressing the oncogene S100A11, leading to enhanced HCC progression.39 In addition, an upregulation of SUV39H1 was evident in both HBV-infected humanized mouse livers and clinical tissues of HBV-related HCC.40 We additionally noted an elevated expression of SUV39H1 in HCC cells, correlating with poorer survival outcomes in HCC patients. This evidence concerns the gene RPL8 and hepatocellular carcinoma.