Although the role of TLR4 in asthma development is controversial, growing evidence proves that high levels of LPS exert beneficial effect in asthma models due to the induction of a Th1 response while low dose of LPS biases the immune response toward a Th2 phenotype and results in aggravation of experimental asthma [17], [18]. The gene discussed is TLR4; the disease is asthma.