Previous studies have shown that high fructose intake facilitates the initiation and progression of HCC in in vivo models with a complex tumor microenvironment.34,54 Furthermore, fructose metabolism plays a critical role in shaping cancer cell invasion and migration phenotypes.55–57 Fructose uptake and metabolism in vascular endothelial cells activate the Akt and Src signaling pathways, thereby significantly enhancing endothelial cell proliferation, migration, and tube formation.56 In this study, we identified a positive role of fructose metabolism in drug-resistant HCC cells. The gene discussed is AKT1; the disease is neoplasm.