Recently, functional in vivo studies identified the TNF superfamily cytokine Tumor necrosis factor-like weak inducer of apoptosis (TWEAK, Apo3L or TNFSF12) as a key contributor to proteinuric kidney disease in the context of immune-complex deposition (lupus nephritis, anti-glomerular basement membrane disease) and in the absence of immune-mediated injury (protein overload)4, 5, 6, 7, 8. Here, TNFSF12 is linked to lupus nephritis.