Given that upregulation of glomerular Toll-like receptor 3 (TLR3) signaling plays a pivotal role in the pathogenesis of LN, we examined whether CQ and HCQ affect the expression of the TLR3 signaling-induced representative proinflammatory chemokines, monocyte chemoattractant protein-1 (MCP-1), and C–C motif chemokine ligand 5 (CCL5) in cultured human glomerular endothelial cells (GECs). This evidence concerns the gene CCL2 and lobular neoplasia.