The pathogenic role of TNF as well as the potential benefits of modulating TNF activity has been shown in models of immune complex-mediated glomerulonephritis, lupus nephritis, antineutrophil cytoplasmic antibodies (ANCA-) associated glomerulonephritis, minimal change disease, diabetic nephropathy (DN), acute kidney injury (AKI), obstructive uropathy, and kidney allograft rejection [14, 15, 19, 21, 23–26]. This evidence concerns the gene TNF and glomerulonephritis.