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. This evidence concerns the gene STING1 and heart failure.