IFNAR2 and diabetes mellitus: In both NOD.RIPSOCS1 and STAT1 deficient NOD mice which are significantly protected from diabetes, signaling through all interferon receptors was inhibited, supporting the potential for redundancy in pathogenic function between interferons in autoimmune diabetes (Flodstrom-Tullberg et al., 2003; Chong et al., 2004; Kim et al., 2007).