IFN-I signaling is increased in pediatric SLE, largely due to the presence of plasmacytoid dendritic cells and pathways such as cyclic GMP-AMP synthase–stimulator of interferon genes–TANK-binding kinase 1 and Toll-like receptor (TLR)4/TLR9. The gene discussed is TBK1; the disease is systemic lupus erythematosus.