Activating STING mutations have been implicated in an autoimmune condition known as STING-associated vasculopathy with onset in infancy (SAVI), in which the mutant STING localizes to the Golgi within the fibroblasts of affected patients, which in turn results in the constitutive activation of IFN expression even in the absence of cGAMP stimulation [195]. Here, STING1 is linked to vascular disorder.