However, the initial studies that implicated PRDI-BF1 (and another factor, PRDII-BF1) as direct repressors of type I IFN relied mostly on over expression and more recently, the same group showed that knockdown of PRDI-BF1 or PRDII-BF1 in mouse embryonic fibroblasts and human MG63 cells does not affect IFN-β repression after viral infection, indicating that at least in this system, Blimp1 is dispensable for the repression of IFN-β expression (59). This evidence concerns the gene PRDM1 and viral infectious disease.