Utilize the MHC-I tail as a substrate could be highly immunomodulatory. Lastly, it will be of interest to determine the nature of cytoskeletal components and trafficking machinery in DCs that bind to or associate with the MHC-I tail, potentially in response to one or more of these modifications. These studies open a door toward the exciting possibility of direct pharmacological manipulation of CTL priming responses at the level of antigen presentation, through direct targeting of the MHC-I cytoplasmic tail. A number of transcription factors are involved in the regulation of lipid metabolism in mammals. The expression levels of genes related to fatty acids and cholesterol homeostasis are modulated by sterol regulatory element binding protein. SREBP-1c regulates fatty acid metabolism, Perifosine whereas Chol homeostasis is strictly regulated by SREBP-2. SREBP-2 is responsible for feedback regulation of the intracellular Chol concentration through expression of the LDL receptor and enzymes in the mevalonate pathway. It is suggested that Chol metabolism and neutral lipid metabolism are interconnected, although the complete picture of neutral lipid metabolism remains to be established. Triacylglycerol is synthesized via two pathways, the monoacylglycerol pathway and the glycerol-3-phosphate pathway. The former is predominantly found in the small intestine, while the latter is present in various tissues, including the liver. In the G3P pathway, G3P is acylated twice, by glycerophosphate acyltransferase and acylglycerophosphate acyltransferase. Then the resulting phosphatidic acid is dephosphorylated to generate diacylglycerol by the activity of PA phosphatase, and finally DG is acylated to produce TG by DG acyltransferase. Recently, the genes responsible for the G3P pathway were identified. The lipin protein family consists of three isoforms named lipin-1, -2 and -3 in mammals, and was found to be the Mg2+ -dependent PA phosphatase type 1 enzyme that hydrolyzes PA to produce DG. Lipin-1, a human homolog of fld, which underlies lipodystrophy in the mouse, is expressed at high levels in white adipose tissue, skeletal muscle and testis, and is also detectable in the liver. In the liver, lipin-2 is more highly expressed than lipin-1 and functions as a major PAP-1 catalyst. The expression level of lipin-3 gene is much lower in the liver. The liver is the major organ of neutral lipid metabolism, and it is essential to clarify the regulatory mechanisms for de novo TG synthesis in the liver to understand the pathophysiology of metabolic diseases.