First, the authors followed the response to infection in a strain of mice called 3d, which has a loss-of-function point mutation in UNC93B1 (an endoplasmic reticulum (ER) resident protein that mediates the translocation of the nucleotide-sensing TLRs from the ER to the endolysosomes) and, consequently, is unresponsive to TLR3, TLR7 and TLR9 ligands (TLR8 is believed to be biologically inactive in mice). This evidence concerns the gene TLR7 and infection.