However, the recently reported VPS72-ACTL6A-MYC regulatory axis by Liu et al.14 suggests a non-ubiquitination-dependent mechanism: this complex enhances MYC transcriptional activity (dual-luciferase reporter assays confirmed that knockdown of VPS72 significantly reduced MYC-specific E-box element activity in HCC cells (p<0.01), whereas VPS72 overexpression increased E-box activity (p<0.01)), promotes glycolysis-related gene expression (HK2, LDHA (p<0.01)), and contributes to HCC progression through metabolic reprogramming. This evidence concerns the gene MYC and hepatocellular carcinoma.