The increased prevalence of dyslipidemia in SLE may be due to both steroid therapy and disease-related pathogenetic mechanisms, including increased C-reactive protein levels, cytokine release (e.g., TNF-alpha and IL-6), and antibodies against lipoprotein lipase (LPL) affecting the balance between pro- and antiatherogenic lipoproteins [68]. The gene discussed is LPL; the disease is systemic lupus erythematosus.