Notably, while BRF1 silencing was associated with an overall increased numbers of DEGs in the TLR3-KO cell line, it is noteworthy that several DEGs involved in innate immune responses (LCN2, C1S, C1R, C3), NF-KB pathway (RELB), interferon response (GPB3), responses to herpesviruses (IFI16) and in MAVS pathway (TRIM31 that promotes the aggregation and activation of MAVS during viral infection (Liu et al., 2017)) were uniquely downregulated in TLR3-KO cells deficient in BRF-1 and thereby Pol III activity. This evidence concerns the gene BRF1 and viral infectious disease.