Since autoantigens‐activated CD4+ T cells or CD8+ T cells produce IFN‐γ during the development of SLE, this leads to the reduction of EBI2 expression in monocyte/macrophages, which alleviates its inhibitory effect on STAT activation to produce higher levels of chemokines and cytokines that not only further facilitates lymphocyte activation and IFN‐γ secretion but also promotes differentiation of lymphocytes into TH17, TFH, and plasma cells, reinforcing the development of SLE. This evidence concerns the gene GPR183 and systemic lupus erythematosus.