We found that in patients with SLE: (1) Histone (H2B, H3, H4) and complements (C1q, C2) are significantly upregulated to participate in antigen presentation; (2) HLA-DPA1 and IL-10 are significantly upregulated to participate in cell activation; (3) C1q, C2, CSTG, ELANE, and FcγR are significantly upregulated and involved in tissue injury. This evidence concerns the gene FCGR2A and systemic lupus erythematosus.