Indeed, a recent study suggested that Ifit1 may act a negative regulator of virus-triggered cellular antiviral responses through its binding to STING and disruption of interaction with IPS-1 and TBK1 [47]; Ifit1−/− mice after peripheral infection of WNV-WT and WNV-E218A should therefore have increased inflammation compared to wild type mice. The gene discussed is STING1; the disease is infection.