Whereas the TLR1/TLR2 specific agonist Pam3CSK4 and high levels of the TLR4 ligand E. coli LPS have beneficial effects in asthma animal models most probably due to re-equilibrium of the cytokine pattern and the induction of a Th1 response [12-14], low dose of LPS and the TLR2 ligand peptidoglycan bias the immune response toward a Th2 phenotype and lead to aggravation of experimental asthma [12,15]. The gene discussed is TLR2; the disease is asthma.