One article has proposed that METTL5-USP5-c-Myc, as a novel mechanism, can control aerobic glycolysis and promote tumor growth, providing a potential therapeutic target for treating HCC.8 Similarly, the present study showed that si-USP34 reduced glucose uptake and lactate production in HCC cells by examining indicators related to glycolysis. The gene discussed is USP34; the disease is neoplasm.