Fatty acid synthase (FASN) is a key enzyme in fatty acid synthesis, playing a critical role in immune cell biology and various diseases. This review discusses the regulatory effects of FASN on immune cells and its implications in immune-related diseases. FASN is involved in the survival, differentiation, and function of immune cells, contributing to the development of immune-related diseases. Dysregulation of FASN is associated with the occurrence and progression of diseases such as tumors, cardiovascular diseases, inflammatory diseases, and autoimmune diseases. Targeting FASN has emerged as a promising therapeutic approach for these conditions. FASN expression is regulated by various factors, including transcription factors like SREBP, the PI3K-AKT signaling pathway, and noncoding RNAs. SREBP activates FASN expression by recognizing its promoter, while the PI3K-AKT pathway influences FASN expression and activity. Noncoding RNAs, such as miRNAs, can regulate FASN expression by targeting FASN or SREBP. Other proteins, including Eif6, USP38, PHLPP1, and GNPAT, also regulate FASN expression and stability. FASN plays a significant role in the polarization and activation of macrophages, particularly M1 macrophages, and influences their function and chemotaxis. It is also involved in the regulation of T lymphocytes, including Th17 cells, Tregs, and other subsets, affecting their differentiation, activation, and function. FASN contributes to the pro-inflammatory role of macrophages and T cells, and its inhibition can reduce inflammation and promote immune responses. In tumors, FASN is involved in the progression of cancer by regulating the tumor microenvironment and immune cell function. FASN inhibition can enhance antitumor immunity by reducing the suppressive effects of Tregs and M2 macrophages. In infectious diseases, FASN is involved in viral replication and host immune response. In autoimmune diseases, FASN is implicated in the pathogenesis of conditions such as multiple sclerosis and rheumatoid arthritis. In inflammatory bowel disease, FASN contributes to the pathogenesis by affecting intestinal barrier function and inflammation. In diabetes, FASN is associated with insulin resistance and metabolic dysfunction. In nonalcoholic fatty liver disease, FASN is involved in the progression of the disease by promoting inflammation and fibrosis. In atherosclerosis, FASN contributes to the development of the disease by promoting lipid accumulation and inflammation. Overall, FASN is a key regulator in immune cell biology and various diseases. Targeting FASN offers potential therapeutic strategies for immune-related diseases, but further research is needed to fully understand its mechanisms and develop effective treatments.Fatty acid synthase (FASN) is a key enzyme in fatty acid synthesis, playing a critical role in immune cell biology and various diseases. This review discusses the regulatory effects of FASN on immune cells and its implications in immune-related diseases. FASN is involved in the survival, differentiation, and function of immune cells, contributing to the development of immune-related diseases. Dysregulation of FASN is associated with the occurrence and progression of diseases such as tumors, cardiovascular diseases, inflammatory diseases, and autoimmune diseases. Targeting FASN has emerged as a promising therapeutic approach for these conditions. FASN expression is regulated by various factors, including transcription factors like SREBP, the PI3K-AKT signaling pathway, and noncoding RNAs. SREBP activates FASN expression by recognizing its promoter, while the PI3K-AKT pathway influences FASN expression and activity. Noncoding RNAs, such as miRNAs, can regulate FASN expression by targeting FASN or SREBP. Other proteins, including Eif6, USP38, PHLPP1, and GNPAT, also regulate FASN expression and stability. FASN plays a significant role in the polarization and activation of macrophages, particularly M1 macrophages, and influences their function and chemotaxis. It is also involved in the regulation of T lymphocytes, including Th17 cells, Tregs, and other subsets, affecting their differentiation, activation, and function. FASN contributes to the pro-inflammatory role of macrophages and T cells, and its inhibition can reduce inflammation and promote immune responses. In tumors, FASN is involved in the progression of cancer by regulating the tumor microenvironment and immune cell function. FASN inhibition can enhance antitumor immunity by reducing the suppressive effects of Tregs and M2 macrophages. In infectious diseases, FASN is involved in viral replication and host immune response. In autoimmune diseases, FASN is implicated in the pathogenesis of conditions such as multiple sclerosis and rheumatoid arthritis. In inflammatory bowel disease, FASN contributes to the pathogenesis by affecting intestinal barrier function and inflammation. In diabetes, FASN is associated with insulin resistance and metabolic dysfunction. In nonalcoholic fatty liver disease, FASN is involved in the progression of the disease by promoting inflammation and fibrosis. In atherosclerosis, FASN contributes to the development of the disease by promoting lipid accumulation and inflammation. Overall, FASN is a key regulator in immune cell biology and various diseases. Targeting FASN offers potential therapeutic strategies for immune-related diseases, but further research is needed to fully understand its mechanisms and develop effective treatments.