Although the extrarenal source of IFN-I is critical in the immunopathogenesis of lupus nephritis (30), importantly, local resident cells, such as mesangial cells, podocytes, tubular epithelial cells and endothelial cells, rather than infiltrating immune cells and hematologic cells, are the major sources of IFN-α in the kidney and are responsible for IFN-α-mediated renal damage in SLE patients (28, 31, 32). This evidence concerns the gene IFNA2 and lupus nephritis.