Immune surveillance and cancer metabolism are closely linked, as tumor cells reprogram their nutrient acquisition and metabolic pathways to meet their energy, biosynthetic, and redox needs. Similarly, immune cells' metabolic processes support host immunity against cancer and determine the differentiation and fate of leukocytes. Metabolic deregulation in immune cells within the tumor microenvironment (TME) can drive immune evasion and compromise therapeutic outcomes. Emerging evidence suggests that anti-tumor immunity can modulate tumor heterogeneity, aggressiveness, and metabolic reprogramming, indicating that immunosurveillance can influence cancer progression in multiple ways. This review summarizes current understanding of how metabolic crosstalk within tumors affects tumor cell immunogenicity and promotes cancer progression. It also explains how defects in the metabolic cascade can lead to dysfunctional immune responses against cancer and discusses the role of immunosuppression as a feedback mechanism. Finally, it highlights ongoing clinical trials and new therapeutic strategies targeting cellular metabolism in cancer. Keywords: Immunodetiring; Immunometabolism; Cancer Evolution Subject Categories: Cancer; Immunology; Metabolism The TME forms a metabolic barrier due to metabolic deregulation in tumor cells, which can disarm host anti-tumor immunity and current immunotherapeutic strategies. Metabolic dysregulation in tumors is a hallmark of cancer. In the past, metabolic activities were considered to support unconstrained growth and anti-apoptosis in tumor cells. Metastatic tumor cells with unique metabolic abilities can potentiate their colonization at secondary sites. Tumor cells have a high metabolic rate, but the TME often lacks proper blood flow and experiences changes in fluid pressure, leading to cells struggling to obtain nutrition and oxygen. However, tumor cells can alter their metabolism to adapt to their environment and support their bioenergetic needs. Tumor cells can change their physiological traits, such as metabolism and stemness properties, through interactions with immune and stromal cells to avoid detection by the immune system. Tumor-derived metabolites can influence the makeup of metastatic niches and the behavior of T cells by rewiring the epigenetic landscape. Tumor cells can alter the metabolic state of the TME or adapt their metabolism to overcome unfavorable conditions, such as nutrient scarcity and immune surveillance. This review discusses the effects of bidirectional metabolic crosstalk between tumor cells and infiltrating immune cells on immune suppression and metabolic adaptation of cancer cells during immunosurveillance derived from the innate and adaptive arms of the immune system, with a focus on T cells, regulatory T cells (Tregs), and natural killer (NK) cells. Intrinsic mutations drive specific nutrient dependencies during cancer progression. Oncogenic mutations that dictate nutrient requirements of cancer cells among different cancer types and organs have been identified. Alterations in oncogenes and tumor suppressor genes regulate amino acid homeostasis and cellular response to nutrient stress, contributing to an immune profile shift within a tumor and to the response to immune therapy. For example, activating the PIImmune surveillance and cancer metabolism are closely linked, as tumor cells reprogram their nutrient acquisition and metabolic pathways to meet their energy, biosynthetic, and redox needs. Similarly, immune cells' metabolic processes support host immunity against cancer and determine the differentiation and fate of leukocytes. Metabolic deregulation in immune cells within the tumor microenvironment (TME) can drive immune evasion and compromise therapeutic outcomes. Emerging evidence suggests that anti-tumor immunity can modulate tumor heterogeneity, aggressiveness, and metabolic reprogramming, indicating that immunosurveillance can influence cancer progression in multiple ways. This review summarizes current understanding of how metabolic crosstalk within tumors affects tumor cell immunogenicity and promotes cancer progression. It also explains how defects in the metabolic cascade can lead to dysfunctional immune responses against cancer and discusses the role of immunosuppression as a feedback mechanism. Finally, it highlights ongoing clinical trials and new therapeutic strategies targeting cellular metabolism in cancer. Keywords: Immunodetiring; Immunometabolism; Cancer Evolution Subject Categories: Cancer; Immunology; Metabolism The TME forms a metabolic barrier due to metabolic deregulation in tumor cells, which can disarm host anti-tumor immunity and current immunotherapeutic strategies. Metabolic dysregulation in tumors is a hallmark of cancer. In the past, metabolic activities were considered to support unconstrained growth and anti-apoptosis in tumor cells. Metastatic tumor cells with unique metabolic abilities can potentiate their colonization at secondary sites. Tumor cells have a high metabolic rate, but the TME often lacks proper blood flow and experiences changes in fluid pressure, leading to cells struggling to obtain nutrition and oxygen. However, tumor cells can alter their metabolism to adapt to their environment and support their bioenergetic needs. Tumor cells can change their physiological traits, such as metabolism and stemness properties, through interactions with immune and stromal cells to avoid detection by the immune system. Tumor-derived metabolites can influence the makeup of metastatic niches and the behavior of T cells by rewiring the epigenetic landscape. Tumor cells can alter the metabolic state of the TME or adapt their metabolism to overcome unfavorable conditions, such as nutrient scarcity and immune surveillance. This review discusses the effects of bidirectional metabolic crosstalk between tumor cells and infiltrating immune cells on immune suppression and metabolic adaptation of cancer cells during immunosurveillance derived from the innate and adaptive arms of the immune system, with a focus on T cells, regulatory T cells (Tregs), and natural killer (NK) cells. Intrinsic mutations drive specific nutrient dependencies during cancer progression. Oncogenic mutations that dictate nutrient requirements of cancer cells among different cancer types and organs have been identified. Alterations in oncogenes and tumor suppressor genes regulate amino acid homeostasis and cellular response to nutrient stress, contributing to an immune profile shift within a tumor and to the response to immune therapy. For example, activating the PI