Strikingly, in the context of the autoinflammatory disease termed STING‐associated vasculopathy with onset in infancy (SAVI), autoactivating STING mutations mimic the structure and location of ligand‐activated STING, positioning STING at the Golgi to drive constitutive signalling (Dobbs et al, 2015; Ergun et al, 2019). The gene discussed is STING1; the disease is STING-associated vasculopathy with onset in infancy.