While NIK SMI1 will likely inhibit more than just TWEAK signaling in vivo, an interpretation in which disease improvement is largely due to inhibition of TWEAK signaling would nevertheless be consistent with a body of literature demonstrating that TWEAK/TWEAKR (Fn14) blockade or deficiency significantly reduce kidney disease in lupus nephritis as well as in other inflammatory preclinical models62–64. Here, TNFRSF12A is linked to lupus nephritis.