To confirm a direct role of TNF-α on migration of SLE BMSCs, recombinant human TNF-α (50 μg/L, 100 μg/L) was added to the cultures, and significant decrease in average healed gaps of SLE BMSCs (247.1765 ± 27.1765 μm versus 190.7647 ± 22.5700 μm, n = 6), and cell migration rate (4.56 ± 0.51‰ versus 3.24 ± 0.37‰, n = 6) (Figure 2(c)) was detected as compared to those without TNF-α treatment, suggesting that TNF-α is an important antagonist for SLE BMSCs migration. This evidence concerns the gene TNF and systemic lupus erythematosus.