Knockdown of NLRX1 leads to enhanced transcription levels of IFNb1, STAT2, and the 2′-5′-oligoadenylate synthetase 1 gene (OAS1) after viral infection, suggesting a negative regulatory role of NLRX1 on the IFN-β/STAT2/OAS1 axis [138]. The gene discussed is NLRX1; the disease is viral infectious disease.