By using a Zf TLR2 mutant (TLR2sa19423 mutant, homozygous (−/−), heterozygous (+/−), and WT (+/+) as control), these authors were able to demonstrate that the mutants with non-functional TLR2 exhibited increased susceptibility to infection, decreased expression of important inflammatory genes such as those involved in chemokine signaling, and decreased granuloma formation [71]. This evidence concerns the gene TLR2 and infection.