The article discusses the role of fatty acid (FA) metabolism in cancer cell proliferation and explores strategies to limit FA availability as a potential therapeutic approach. Cancer cells exhibit altered metabolism, including the Warburg effect, where they prefer glycolysis over oxidative phosphorylation despite oxygen availability. Additionally, increased glutamine metabolism and changes in lipid metabolism are observed in cancer cells. Fatty acids are essential for membrane synthesis, signaling molecules, and energy storage in cancer cells, making their metabolism a critical factor in cancer progression. The article highlights that cancer cells often synthesize fatty acids de novo, relying on enzymes such as ATP citrate lyase (ACLY), acetyl-CoA carboxylase (ACC), fatty acid synthase (FASN), and others. Limiting FA availability through inhibition of these enzymes or by altering FA metabolism can reduce cancer cell proliferation. For instance, inhibiting ACLY, ACC, or FASN has shown anti-tumor effects in various cancer models. Additionally, the role of fatty acid transporters like CD36 and fatty acid-binding protein 4 (FABP4) in cancer cell metabolism is discussed. The review also covers the regulation of FA metabolism by transcription factors such as SREBP-1, which controls the expression of genes involved in FA synthesis. Inhibiting SREBP-1 or its downstream targets can reduce FA synthesis and promote cancer cell death. Furthermore, increasing FA degradation through mitochondrial β-oxidation or diverting FAs to storage in lipid droplets is explored as a potential strategy to limit FA availability for cancer cell growth. The article emphasizes the complexity of lipid metabolism in cancer, noting that many enzymes involved in FA metabolism have multiple isoforms with distinct functions. This complexity underscores the need for targeted therapies that consider the specific metabolic requirements of different cancer types. Overall, the review provides a comprehensive overview of FA metabolism in cancer and highlights the potential of targeting FA metabolism as a therapeutic strategy.The article discusses the role of fatty acid (FA) metabolism in cancer cell proliferation and explores strategies to limit FA availability as a potential therapeutic approach. Cancer cells exhibit altered metabolism, including the Warburg effect, where they prefer glycolysis over oxidative phosphorylation despite oxygen availability. Additionally, increased glutamine metabolism and changes in lipid metabolism are observed in cancer cells. Fatty acids are essential for membrane synthesis, signaling molecules, and energy storage in cancer cells, making their metabolism a critical factor in cancer progression. The article highlights that cancer cells often synthesize fatty acids de novo, relying on enzymes such as ATP citrate lyase (ACLY), acetyl-CoA carboxylase (ACC), fatty acid synthase (FASN), and others. Limiting FA availability through inhibition of these enzymes or by altering FA metabolism can reduce cancer cell proliferation. For instance, inhibiting ACLY, ACC, or FASN has shown anti-tumor effects in various cancer models. Additionally, the role of fatty acid transporters like CD36 and fatty acid-binding protein 4 (FABP4) in cancer cell metabolism is discussed. The review also covers the regulation of FA metabolism by transcription factors such as SREBP-1, which controls the expression of genes involved in FA synthesis. Inhibiting SREBP-1 or its downstream targets can reduce FA synthesis and promote cancer cell death. Furthermore, increasing FA degradation through mitochondrial β-oxidation or diverting FAs to storage in lipid droplets is explored as a potential strategy to limit FA availability for cancer cell growth. The article emphasizes the complexity of lipid metabolism in cancer, noting that many enzymes involved in FA metabolism have multiple isoforms with distinct functions. This complexity underscores the need for targeted therapies that consider the specific metabolic requirements of different cancer types. Overall, the review provides a comprehensive overview of FA metabolism in cancer and highlights the potential of targeting FA metabolism as a therapeutic strategy.