Abstract: Hepatocellular carcinoma (HCC) is the most common type of primary liver cancer, which is closely associated with multiple factors, including metabolic reprogramming, immune evasion, and changes in the tumor microenvironment. In recent years, abnormal lactate metabolism has been identified as a key factor in the initiation, progression, and immune escape of HCC. Lactate is not merely a byproduct of glycolysis but also acts as a "metabolic signaling molecule" that influences gene expression, immune responses, and cell fate through post‑translational modifications such as lactylation. The accumulation of lactate in HCC not only promotes tumor cell proliferation and metas-tasis but also suppresses the activity of immune effector cells by altering the tumor microenviron-ment, thereby facilitating tumor immune evasion. The authors summarize the mechanisms of lactate metabolism and lactylation in HCC, discuss their potential as therapeutic targets, aiming to provide new insights and strategies for liver cancer treatment.