Similarly, our study found that treatment with DSF/Cu resulted in the downregulation of Bcl-2 and upregulation of Bax, Cytochrome c, Cleaved caspase 3, and 9 in hepatocellular carcinoma cell lines, indicating that DSF/Cu not only induced mitochondrial damage dysfunction but also promoted HCC cell apoptosis, thereby inhibiting tumor progression. Here, BAX is linked to hepatocellular carcinoma.