GSEA also confirmed the upregulation of several proinflammatory pathways, including TNFα via NF-κB, and JAK/STAT signaling in SAVI patient T and B cells (Fig. 2 D and Fig. S1 D), as well as significant modulation of other pathways related to DNA damage, proliferation, and cell death, previously reported to be dependent of STING activation (Wu et al., 2020; Hong et al., 2022; Fremond et al., 2021) (Fig. 2 D). The gene discussed is SOAT1; the disease is STING-associated vasculopathy with onset in infancy.