Although DCs are activated by Type I IFNs (Gallucci et al., 1999), and might therefore become hyperactivated, and thus initiate the autoimmune process, phenotypic, or specific functional abnormalities of DCs in Trex1−/− mice or in patients with Aicardi–Goutières syndrome have not yet been reported. The gene discussed is TREX1; the disease is Aicardi-Goutieres syndrome.