However, 24 h post infection, we observed overall increased systemic cytokine and chemokine levels in mice deficient in endosomal TLR signaling (Figures 5A,B), presumably due to an increased bacteremia, as demonstrated by a tendency toward higher bacterial burden in spleens from Unc93b1 mutant mice compared to their WT counterparts (Supplementary Figure 7). This evidence concerns the gene UNC93B1 and infection.