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). Here, IRF3 is linked to STING-associated vasculopathy with onset in infancy.