The *MYC* oncogene, a transcription factor, plays a crucial role in promoting cell growth and proliferation by triggering selective gene expression amplification. In normal cells, *MYC* is tightly regulated, but in cancer, genetic and epigenetic alterations can silence checkpoints, unleashing *MYC*'s metabolic activities. *MYC* coordinates nutrient acquisition to produce ATP and cellular building blocks, leading to increased cell mass and DNA replication. In cancer, uncontrolled growth creates dependence on *MYC*-driven metabolic pathways, making specific metabolic enzymes novel targets for cancer therapy. *MYC* regulates genes involved in glycolysis, glutaminolysis, nucleotide synthesis, lipid synthesis, and organelle biogenesis, such as ribosomes and mitochondria. It also directly triggers cell cycle progression by activating genes like cyclin D and CDK4. Oncogenic *MYC* rewires metabolism, creating therapeutic vulnerabilities, such as synthetic lethality with specific metabolic enzyme inhibitors.The *MYC* oncogene, a transcription factor, plays a crucial role in promoting cell growth and proliferation by triggering selective gene expression amplification. In normal cells, *MYC* is tightly regulated, but in cancer, genetic and epigenetic alterations can silence checkpoints, unleashing *MYC*'s metabolic activities. *MYC* coordinates nutrient acquisition to produce ATP and cellular building blocks, leading to increased cell mass and DNA replication. In cancer, uncontrolled growth creates dependence on *MYC*-driven metabolic pathways, making specific metabolic enzymes novel targets for cancer therapy. *MYC* regulates genes involved in glycolysis, glutaminolysis, nucleotide synthesis, lipid synthesis, and organelle biogenesis, such as ribosomes and mitochondria. It also directly triggers cell cycle progression by activating genes like cyclin D and CDK4. Oncogenic *MYC* rewires metabolism, creating therapeutic vulnerabilities, such as synthetic lethality with specific metabolic enzyme inhibitors.