The −1237 was also identified by our group as being the site of interaction in which nuclear factor-κBp65/ERα suppressed TLR9 transcription and thus IFN production.20 Earlier findings from our team revealed that Epstein Barr virus infection of primary B cells led to a decrease in TLR9 mRNA levels, which became increasingly distinct upon immortalization, signifying that the reduction in TLR9 expression may be linked to cellular transformation (19). This evidence concerns the gene IFNA1 and Epstein-Barr virus infection.