This review discusses the role of fatty acid (FA) metabolism in cancer cell proliferation and its potential as a therapeutic target. Cancer cells often exhibit altered metabolism, including increased FA synthesis and utilization, which is essential for membrane and signaling molecule production. The Warburg effect, a shift toward glycolysis despite oxygen availability, is a well-known metabolic change in cancer. Additionally, increased glutamine metabolism contributes to FA synthesis. FA metabolism is crucial for cancer cell growth, and limiting FA availability can inhibit proliferation. Several strategies to limit FA availability include blocking FA synthesis, increasing FA degradation, diverting FAs to storage, or reducing FA release from storage. Key enzymes in FA metabolism, such as ATP citrate lyase (ACLY), acetyl-CoA carboxylase (ACC), fatty acid synthase (FASN), and stearoyl-CoA desaturase (SCD), are potential therapeutic targets. Inhibiting these enzymes can reduce FA synthesis and impair cancer cell growth. The transcriptional regulator SREBP-1 controls FA synthesis and is overexpressed in many cancers. Inhibiting SREBP-1 can decrease FA synthesis and promote cancer cell death. Additionally, increasing FA oxidation through CPT1 inhibition or PPARα activation may have therapeutic potential, although results are mixed. Diverting FAs to storage, such as in lipid droplets, may reduce their availability for membrane and signaling functions, thereby inhibiting cancer cell proliferation. Inhibiting FA release from storage, such as through lipases like MAGL, can also limit FA availability. However, the effectiveness of these strategies depends on the specific cancer type and metabolic context. Overall, targeting FA metabolism offers a promising approach to cancer therapy, as it can selectively affect highly proliferative cancer cells while sparing normal cells. Understanding the complex interplay of FA metabolism in different cancers is essential for developing effective therapeutic strategies.This review discusses the role of fatty acid (FA) metabolism in cancer cell proliferation and its potential as a therapeutic target. Cancer cells often exhibit altered metabolism, including increased FA synthesis and utilization, which is essential for membrane and signaling molecule production. The Warburg effect, a shift toward glycolysis despite oxygen availability, is a well-known metabolic change in cancer. Additionally, increased glutamine metabolism contributes to FA synthesis. FA metabolism is crucial for cancer cell growth, and limiting FA availability can inhibit proliferation. Several strategies to limit FA availability include blocking FA synthesis, increasing FA degradation, diverting FAs to storage, or reducing FA release from storage. Key enzymes in FA metabolism, such as ATP citrate lyase (ACLY), acetyl-CoA carboxylase (ACC), fatty acid synthase (FASN), and stearoyl-CoA desaturase (SCD), are potential therapeutic targets. Inhibiting these enzymes can reduce FA synthesis and impair cancer cell growth. The transcriptional regulator SREBP-1 controls FA synthesis and is overexpressed in many cancers. Inhibiting SREBP-1 can decrease FA synthesis and promote cancer cell death. Additionally, increasing FA oxidation through CPT1 inhibition or PPARα activation may have therapeutic potential, although results are mixed. Diverting FAs to storage, such as in lipid droplets, may reduce their availability for membrane and signaling functions, thereby inhibiting cancer cell proliferation. Inhibiting FA release from storage, such as through lipases like MAGL, can also limit FA availability. However, the effectiveness of these strategies depends on the specific cancer type and metabolic context. Overall, targeting FA metabolism offers a promising approach to cancer therapy, as it can selectively affect highly proliferative cancer cells while sparing normal cells. Understanding the complex interplay of FA metabolism in different cancers is essential for developing effective therapeutic strategies.