To study the role of STING in the pathophysiology of the disease, our team (Bouis et al, 2019) and others (Motwani et al, 2019; Warner et al, 2017; Luksch et al, 2019; Bennion et al, 2019; Martin et al, 2019; Siedel et al, 2020; Bennion et al, 2020) developed STING GOF mouse models including mice carrying the heterozygous V154M mutation (Bouis et al, 2019; Motwani et al, 2019), corresponding to the most common human V155M mutation (about 60%) in SAVI patients. This evidence concerns the gene STING1 and STING-associated vasculopathy with onset in infancy.