Purpose of the Review <p>Hepatocellular carcinoma is a type of cancer with high rates of occurrence and death worldwide. Recently, the marked increase in liver cancer risk among patients with metabolic-associated steatotic liver disease has drawn considerable attention to the metabolic-immune evolutionary mechanisms underlying this condition. In this article, we systematically review the main metabolic-immune signaling pathways linked to the advancement of hepatic steatosis, inflammation, and carcinogenesis. This review examines their roles and potential therapeutic significance within the tumor microenvironment, with the objective of furnishing a theoretical foundation and identifying novel therapeutic targets for the precise treatment.</p> Recent Findings <p>The carcinogenic process entails complex and dynamic interactions between energy metabolism and immune cells. The latest studies focusing on metabolic-immune interactions bring attention to significant signaling routes such as PI3K/AKT/mTOR and AMPK. These pathways regulate energy metabolism reprogramming in the HCC microenvironment and facilitate tumor immune evasion, impacting tumor growth and metastasis.</p> Summary <p>Hepatocellular carcinoma significantly contributes to global cancer mortality, with existing treatments showing limited effectiveness, thus heavily burdening public health systems.The carcinogenic process of hepatocellular carcinoma is characterized by a multitude of pathogenic mechanisms, notably the intricate interplay between energy metabolism and immune functions, which involves numerous signaling pathways. Thoroughly analyzing the regulatory mechanisms of these signaling routes could lay a theoretical groundwork for finding new therapeutic targets and bettering the prognosis for hepatocellular carcinoma patients.</p>