Finally, we found that whereas transduction of cells from mice bearing a Blau KI mutation with a lentivirus expressing an empty vector exhibited enhanced IκBα and ERK responses when stimulated via TLR2 or TLR4, infection of cells with an IRF4-expressing lentivirus exhibited reduced capacity to activate IκBα and ERK when similarly stimulated. This evidence concerns the gene NFKBIA and infection.