Indeed, because JAK-STAT inhibitors showed a similar suppressive effect on over-functional STING-induced immune responses, we hypothesize that STAT1 (downstream of STING-IRF3-type I IFN axis), which is constitutively phosphorylated in B and T cells of certain SAVI patients, may act as another potential target, but requires further investigation for the antagonistic binding of HHMX, in addition to TBK1 (19). This evidence concerns the gene TBK1 and STING-associated vasculopathy with onset in infancy.