In this regard, Cys206-dependent STING polymerization favors noncanonical STING activation, which may partially explain the close association between individuals with mutations at Cys206 of STING and SAVI (STING-associated vasculopathy with onset in infancy), a disease characterized by systemic inflammation resulting from constitutive activation of the canonical STING pathway (53, 54). This evidence concerns the gene STING1 and vascular disorder.