Therefore, there is an interest in using anti-inflammatory or edna techniques efficient inventory monitoring programs sensitive species immunomodulatory therapies for this condition. MMF, an immunosuppressive agent, is currently used for the treatment of SLE patients, particularly those with kidney involvement, as well as for the prevention of rejection in transplant patients. MMF was first demonstrated to inhibit T-cell function, however, MMF also exerts inhibitory effects on other immune cells and effectors, including downregulation of cell adhesion molecules and attenuation of monocyte and macrophage responses. MMF has also been shown to suppress a number of the inflammatory events that are involved in the development of atherosclerosis. T-lymphocyte infiltration to atherosclerotic plaque and circulation 
to sites of inflammation is abrogated by MMF treatment. MMF has been shown to reduce the expression of vascular adhesion molecules in atherosclerosis by inhibiting the nuclear factor NFkB which is required for their transcriptional upregulation. Raisanen et al showed that MMF treatment reduces the appearance and proliferation of smooth muscle cells in the intima, which normally contribute to atherosclerotic plaque formation by recruitment of extracellular matrix and self-proliferation. Thus, MMF has properties that could be considered anti-atherogenic: inhibiting T-cells, blocking leukocyte adhesion and inhibiting proliferation of smooth muscle cells; therefore making it a potentially valuable drug to prevent the development of atherosclerosis in patients with SLE. A recent publication examined the effect of MMF on atherosclerosis development by using bone marrow transplantation to generate a mouse model of lupus with associated atherosclerosis. Substantial evidence exists to support a critical role of inflammation in the pathology of both SLE and CVD caused by atherosclerosis. The chronic inflammation associated with SLE correlates to the increased risk in CVD seen in patients. The current study suggests that MMF, in addition to this wellknown efficacy on lupus nephritis, might be a promising agent for the prevention of atherosclerosis in SLE. A more extensive analysis of atherosclerosis and SLE in these MMF-treated gld.apoE2/2 mice will need to be performed to fully determine how MMF impacts the accelerated atherosclerosis of our lupus mouse model and potentially bring a better understanding of the link between atherogenesis and autoimmune disease. The worldwide incidence of obesity has increased dramatically during recent decades. The “thrifty genes”, which were historically advantageous, may now be detrimental due to the abundance of the food supply and dramatic changes in modern lifestyle, and contribute to the major epidemic of obesity. Obesity is associated with a high incidence of steatosis, insulin resistance and chronic inflammation. Obesity-related non-alcoholic fatty liver disease has recently been recognized as one of the major causes of chronic liver disorders, estimated to affect at least one-quarter of the general population. NAFLD is characterized by excess liver lipid accumulation, hepatic insulin resistance, and later hepatic inflammation, leading to nonalcoholic steatohepatitis and culminating in hepatic fibrosis or cirrhosis. One of the major causes of fat accumulation in NAFLD is the inability of the liver to regulate the changes in lipogenesis in the transition from fasted to fed state. Several studies suggested that hepatic lipogenesis is increased in hepatic steatosis, which may result from either increased triglyceride synthesis or decreased fatty acid oxidation through production of malonyl- CoA, both leading to increased triglyceride content in the liver. Excess fat accumulation ultimately leads to hepatic steatosis and worsening hepatic insulin resistance via a network of transcription factors, which regulate hepatic lipogenesis and fatty acid oxidation.