Mechanisms such as tumor necrosis factor-alpha (TNF-α)-mediated inhibition of lipoprotein lipase, low lipoprotein activity, and the presence of antibodies to lipoprotein lipase found in patients with SLE have been suggested to contribute to the pathophysiology of dyslipidemia in SLE (41, 43). The gene discussed is TNF; the disease is systemic lupus erythematosus.