UNC93B1 and glomerulonephritis: For example, TLR9‐deficient mice exhibit clear lupus‐like clinical manifestations158 and TLR9−/− autoimmune‐prone MRL/lpr animals have a shorter lifespan due to severe SLE and glomerulonephritis.4 Consistent with these results, another study has proposed that TLR9 acts as a negative regulator of TLR7, the main culprit of SLE pathogenesis,158 by competing for UNC93B1 in the ER.159, 160 Indeed, a point mutation in UNC93B1 (D34A) facilitates the association with TLR7 and dampens TLR9 activity, leading to severe systemic inflammation in Unc93b1D34A/D34A mice.160