STING1 and atrophic macular degeneration: In mice lacking either of these DNases, cGAS is activated by self-DNA and the mice develop severe autoimmune diseases.24,25 Similarly, patients with gain-of-function mutations in STING or loss-of-function mutations in TREX1 or DNase II showed an overactive cGAS-STING pathway and severe autoimmune phenotypes.26,27 Additional studies found that cGAS is involved in diseases characterized by “sterile inflammation” such as heart failure, fibrosis, geographic atrophy, and cancer.28–30