It has been demonstrated that the inflammatory microenvironment of SLE patients with lupus nephritis increases NF-κB expression in the glomerular endothelial and mesangial cells, and overexpression of NF-κB could induce expression of inflammatory cytokines, chemokines, adhesion molecules, and inflammatory enzymes in turn, causing a vicious cycle [15]. Here, NFKB1 is linked to lupus nephritis.