This review discusses the role of MYC in cancer metabolism and oncoimmunology, highlighting its dual functions in regulating cellular metabolism and immune evasion. MYC is a transcription factor that governs various cellular processes, including cell proliferation, DNA repair, and metabolism. It interacts with multiple partners and cofactors to regulate gene expression, influencing both metabolic reprogramming and immune evasion. Recent studies have shown that MYC promotes glucose and glutamine metabolism, which supports cancer cell proliferation and survival. Additionally, MYC influences the activation of antigen presentation on regulatory T cells, contributing to immune evasion. MYC is involved in the regulation of key metabolic pathways, including glycolysis and amino acid metabolism. It also plays a critical role in immune evasion by modulating the expression of immune checkpoint molecules and self-antigens, thereby suppressing immune recognition of cancer cells. The interplay between MYC and HIF-1α is particularly important, as both regulate metabolic reprogramming and immune evasion. MYC also influences the tumor microenvironment by recruiting pro-tumoral macrophages and promoting immunosuppressive conditions. Despite its importance, MYC has been considered "undruggable" due to its lack of enzymatic activity and the difficulty in targeting it directly. However, recent advances in understanding the MYC interactome have led to the development of therapeutic strategies, including small molecule inhibitors and peptides that disrupt MYC-MAX interactions. Omomyc, a MAX-interfering peptide, has shown promise in preclinical models and is currently being tested in clinical trials for various cancers. This review emphasizes the need for further research into MYC-targeted therapies, particularly in the context of oncometabolism and oncoimmunology. The development of effective therapeutic strategies that target MYC's role in both metabolic reprogramming and immune evasion is crucial for improving cancer treatment outcomes. The review also highlights the potential of combining direct and indirect approaches to inhibit MYC, which could lead to more effective and comprehensive cancer therapies.This review discusses the role of MYC in cancer metabolism and oncoimmunology, highlighting its dual functions in regulating cellular metabolism and immune evasion. MYC is a transcription factor that governs various cellular processes, including cell proliferation, DNA repair, and metabolism. It interacts with multiple partners and cofactors to regulate gene expression, influencing both metabolic reprogramming and immune evasion. Recent studies have shown that MYC promotes glucose and glutamine metabolism, which supports cancer cell proliferation and survival. Additionally, MYC influences the activation of antigen presentation on regulatory T cells, contributing to immune evasion. MYC is involved in the regulation of key metabolic pathways, including glycolysis and amino acid metabolism. It also plays a critical role in immune evasion by modulating the expression of immune checkpoint molecules and self-antigens, thereby suppressing immune recognition of cancer cells. The interplay between MYC and HIF-1α is particularly important, as both regulate metabolic reprogramming and immune evasion. MYC also influences the tumor microenvironment by recruiting pro-tumoral macrophages and promoting immunosuppressive conditions. Despite its importance, MYC has been considered "undruggable" due to its lack of enzymatic activity and the difficulty in targeting it directly. However, recent advances in understanding the MYC interactome have led to the development of therapeutic strategies, including small molecule inhibitors and peptides that disrupt MYC-MAX interactions. Omomyc, a MAX-interfering peptide, has shown promise in preclinical models and is currently being tested in clinical trials for various cancers. This review emphasizes the need for further research into MYC-targeted therapies, particularly in the context of oncometabolism and oncoimmunology. The development of effective therapeutic strategies that target MYC's role in both metabolic reprogramming and immune evasion is crucial for improving cancer treatment outcomes. The review also highlights the potential of combining direct and indirect approaches to inhibit MYC, which could lead to more effective and comprehensive cancer therapies.