Consistent with observations in the literature, demonstrating a role for A20 in inhibiting STAT1 and showing higher circulating levels of IFNγ inducible chemokines in patients with HA20 and in A20 genetically deficient mice (10, 11), all our patients showed markedly higher circulating levels of CXCL9 and CXCL10 compared to healthy donors (Figure 4A). This evidence concerns the gene CXCL9 and A20 haploinsufficiency.