Although cGAS-STING activation is typically induced by DNA derived from pathogenic microbes or viruses, excessive self-DNA derived from apoptosis-derived membrane vesicles (9), neutrophil extracellular traps (NETs) (10), and mitochondrial DNA (11, 12) shed into the cytoplasm are increased in SLE and activate the cGAS-STING pathway. The gene discussed is STING1; the disease is systemic lupus erythematosus.