Because SLE is associated with an increased risk of cardiovascular disease (59) and because we had previously shown that myeloid-targeted ACSL1-deficiency results in smaller early lesions of atherosclerosis due to reduced macrophage accumulation in a mouse model of type 1 diabetes (another autoimmune disease associated with increased IFN signaling) (6, 25), we used LDL receptor-deficient (Ldlr−/−) mice to allow analysis of atherosclerosis. This evidence concerns the gene IFNA1 and systemic lupus erythematosus.