TNF-α at different concentrations significantly downregulated the migration capacity of SLE BMSCs, while anti-TNF-α mAb ameliorated SLE serum induced inhibition of SLE BMSCs migration, suggesting the elevation of TNF-α in SLE patients could be involved in this process, which was quite contrary to the result in BMSCs from healthy controls [11–13]. The gene discussed is TNF; the disease is systemic lupus erythematosus.