As maladaptive inflammation plays a key role in amplifying renal injury, NF-κB or related pathways that activate NF-κB, like the TBK1/IKKε/TI-IFN pathway which we now characterized, may contribute to interferon-related nephropathies, and become therapeutic targets (Sanz et al., 2010b; Markó et al., 2016; Gianassi et al., 2019; Song et al., 2019). This evidence concerns the gene NFKB1 and kidney disorder.