While activating mutations in the STING protein have been identified in patients with the autoinflammatory disorder STING-associated vasculopathy with onset in infancy (SAVI)18,19, it is becoming increasingly clear that dysregulation of STING trafficking, especially post-Golgi, can similarly cause disease with a STING-dependent autoinflammatory component. This evidence concerns the gene STING1 and STING-associated vasculopathy with onset in infancy.