After sulfasalazine, the expression level of SLC7A11 was significantly downregulated (Supplementary figure 6), the Fe2+ signal (Figures 3(h) and 3(i)) and lipid peroxidation (Figures 3(j) and 3(k)) was significantly increased in B cells isolated from lupus mouse, meanwhile the intracellular GSSH and GSH were also altered accordingly (Figures 3(l) and 3(m)), indicating IL-6 facilitates ferroptosis resistance in lupus B cells via SLC7A11. This evidence concerns the gene SLC7A11 and systemic lupus erythematosus.