USP22 controls nuclear accumulation of IRF3 and type I IFN signaling through KPNA2 deubiquitination only upon infection with SeV and HSV-1 and loss of USP22 expression decreased type I IFN responses upon virus infection, while USP22 deletion in uninfected cells did not trigger basal IFN signaling [54]. This evidence concerns the gene USP22 and viral infectious disease.