Two other studies found that infection of hSTAT2-KI mice with ZIKV did not only recapitulate the extreme vulnerability and lethality of mice lacking the interferon receptor (IFNAR1−/−; Lazear et al., 2016) or STAT2 (STAT2−/− mice; Tripathi et al., 2017), but also reflect the cell-extrinsic antiviral effects of IFN signaling (Yang et al., 2024). The gene discussed is IFNAR1; the disease is infection.