HMGB1 can activate and chemotacticize inflammatory cells, participate in TLR4 mediated immune responses, activate nuclear factor kappa-B (NF-κB) through Myeloid differentiation primary response 88 (MyD88), lead to the release of inflammatory factors, and thus promote the development and progression of SLE and atherosclerosis (Porto et al., 2006; Xiao et al., 2016). This evidence concerns the gene TLR4 and atherosclerosis.