A study has shown that when USP25 was upregulated by virus infection or LPS, IRF 7 could directly bind to two conserved IRF binding sites on the USP25 promoter, driving the transcription of USP25 and promoting the secretion of IFN-Is to adjust the innate immune signal transduction and exhibit an anti-inflammatory effect [114]. The gene discussed is USP25; the disease is viral infectious disease.