UNC93B1 and autoimmune disease: To support the interaction between TLR7 and TLR9 upon the development of autoimmune disease, Fukui et al. generated Unc93B1D34A/D34A knock-in mice to show that TLR9 competes with TLR7 for binding to Unc93B1 in the healthy state, while TLR7 is constitutively activated upon autoinflammatory responses because TLR9 has a lower affinity for the Unc93B1-like Unc93B1D34A/D34A mutant (Fukui et al., 2011).