Our earlier studies had shown that autoimmunity and glomerulonephritis in ABIN1[D485N] mice were prevented by crossing to MyD88 KO mice (Nanda et al, 2011) or mice expressing kinase-inactive mutants of IRAK4 or IRAK1 (Nanda et al, 2016). This evidence concerns the gene IRAK1 and glomerulonephritis.