This activation is a hallmark of several autoinflammatory and autoimmune conditions, including systemic lupus erythematosus (SLE), Aicardi-Goutières syndrome, and STING-associated vasculopathy with onset in infancy (SAVI), where disrupted IFN signaling drives pathological immune activation and tissue damage (3, 11, 12). This evidence concerns the gene STING1 and systemic lupus erythematosus.