While antagonizing CD40L with anti-CD40L in LDL-receptor deficient mice has been shown to cause substantial reductions of atherosclerotic lesions and their lipid content, and the amount of intralesional macrophages and T cells, as well as VCAM-1 expression on the endothelium [98], a clinical trial testing anti-CD40L in patients with SLE was unfortunately terminated prematurely due to excessive occurrence of cardiovascular events [99]. This evidence concerns the gene CD40LG and systemic lupus erythematosus.