For example, TREX1, a DNA exonuclease, is frequently mutated in human patients with AGS and systemic lupus erythematosus (SLE) 89, 90, 91, and co‐deletion of cGAS, STING, Interferon‐α/β receptor (IFNAR) or IRF3 rescues this phenotype 92, 93, 94, 95, 96, 97, 98. Here, IFNAR1 is linked to systemic lupus erythematosus.