Enhanced TLR7 signaling is central to SLE pathogenesis through (1) increased TLR7 expression via gene duplication or stabilizing SNPs, (2) sustained activation by endosomal ligand accumulation, and (3) gain-of-function mutations lowering activation thresholds [47,63,69,91]. The gene discussed is TLR7; the disease is systemic lupus erythematosus.