The review discusses the intricate relationship between tumor metabolism and immunosurveillance, highlighting how metabolic crosstalk between tumor cells and immune cells influences tumor progression and immune evasion. It begins by explaining how tumor cells reprogram their metabolic pathways to meet their energetic, biosynthetic, and redox demands, while immune cells support host immunity through metabolic processes. The review then delves into how metabolic deregulation in immune cells within the tumor microenvironment can drive immune evasion and compromise therapeutic outcomes. It also explores how anti-tumor immunity can modulate tumor heterogeneity, aggressiveness, and metabolic reprogramming, suggesting that immunosurveillance can instruct cancer progression in multiple dimensions. The review further examines how intrinsic mutations drive specific nutrient dependencies in cancer cells, contributing to immune profile shifts and response to immune therapy. It discusses the role of metabolic enzymes in epigenetic regulation and how mutations in these enzymes can impact cancer aggressiveness. The tissue origin of tumors is also considered, noting that the metabolic preferences of tumor cells can vary even when carrying the same mutations, influenced by the local microenvironment. The review highlights the metabolic plasticity and flexibility of cancer cells, which allows them to survive under stressful conditions. It explains how tumor cells can alter their metabolism to adapt to nutrient scarcity and immune surveillance, and how this affects the function of immune cells such as T cells, regulatory T cells (Tregs), and natural killer (NK) cells. The review also discusses the metabolic properties of metastases and the metastatic niche, emphasizing how metabolic reprogramming contributes to metastasis and immune evasion. Finally, the review explores the interplay between cancer cells and infiltrating immune cells, particularly the role of glucose competition in driving an immunosuppressive tumor microenvironment. It discusses how amino acid metabolism and fatty acid and lipid metabolism influence lymphocyte differentiation and function, and how these metabolic interactions contribute to tumor heterogeneity and immune surveillance. The review concludes by highlighting ongoing clinical trials and new therapeutic strategies targeting cellular metabolism in cancer.The review discusses the intricate relationship between tumor metabolism and immunosurveillance, highlighting how metabolic crosstalk between tumor cells and immune cells influences tumor progression and immune evasion. It begins by explaining how tumor cells reprogram their metabolic pathways to meet their energetic, biosynthetic, and redox demands, while immune cells support host immunity through metabolic processes. The review then delves into how metabolic deregulation in immune cells within the tumor microenvironment can drive immune evasion and compromise therapeutic outcomes. It also explores how anti-tumor immunity can modulate tumor heterogeneity, aggressiveness, and metabolic reprogramming, suggesting that immunosurveillance can instruct cancer progression in multiple dimensions. The review further examines how intrinsic mutations drive specific nutrient dependencies in cancer cells, contributing to immune profile shifts and response to immune therapy. It discusses the role of metabolic enzymes in epigenetic regulation and how mutations in these enzymes can impact cancer aggressiveness. The tissue origin of tumors is also considered, noting that the metabolic preferences of tumor cells can vary even when carrying the same mutations, influenced by the local microenvironment. The review highlights the metabolic plasticity and flexibility of cancer cells, which allows them to survive under stressful conditions. It explains how tumor cells can alter their metabolism to adapt to nutrient scarcity and immune surveillance, and how this affects the function of immune cells such as T cells, regulatory T cells (Tregs), and natural killer (NK) cells. The review also discusses the metabolic properties of metastases and the metastatic niche, emphasizing how metabolic reprogramming contributes to metastasis and immune evasion. Finally, the review explores the interplay between cancer cells and infiltrating immune cells, particularly the role of glucose competition in driving an immunosuppressive tumor microenvironment. It discusses how amino acid metabolism and fatty acid and lipid metabolism influence lymphocyte differentiation and function, and how these metabolic interactions contribute to tumor heterogeneity and immune surveillance. The review concludes by highlighting ongoing clinical trials and new therapeutic strategies targeting cellular metabolism in cancer.