Considering that, in SLE, the production of autoantibodies is a hallmark of this autoimmune disease, it has been noticed that specific autoantibodies contribute to atherosclerosis in pathology, such as anti-HDL-IgG related to induce LDL to enter the endothelial cells (EC) and anti-apolipoprotein A1 (ApoA1)-IgG, which induces the activation of NF-kB and favors the expression of inflammatory factors, among which are TNF-α, interleukin-6 (IL-6), interleukin-8 (IL-8), C-C motif chemokine ligand 2 (CCL2), and metalloproteinase 9 [32]. The gene discussed is APOA1; the disease is atherosclerosis.