After ligand binding, the preformed dimer undergoes conformational changes that trigger an intracellular signaling cascade that leads to the activation of NF‐κB and the secretion of pro‐inflammatory cytokines like tumor necrosis factor (TNF) and interleukin (IL)‐8.3 Under certain circumstances this response is excessive and leads to severe conditions like sepsis, rheumatoid arthritis, autoimmune diabetes, asthma and certain types of allergies.1, 4 The modulation of TLR2 function by small molecules has been postulated as a promising strategy to treat these conditions. The gene discussed is TNF; the disease is asthma.