Furthermore, OXA treatment led to a significant reduction in chemokines (CCL2, CCL4, CCL5, CXCL9, and CXCL12) and cytokines (IFN-γ, TNF-α, IL-16, IL-17, IL-23, IL-27, and colony-stimulating factor 1 (CSF1)), involved in pathogenesis of lupus glomerulonephritis, in kidneys of OXA-treated SLE mice, as well as a reduction in kidney damage and immune cell infiltration (T cells, monocytes, macrophages, and B cells) into the kidneys. The gene discussed is CSF1; the disease is lupus nephritis.