41 showed that primary bronchial epithelial cells from asthma patients were able to up‐regulate TLR3, following infection, but failed to initiate an effective innate immune response. Deifl et al. stimulated in vitro monocytes and monocyte‐derived dendritic cells from allergic patients with TLR ligands. They found that TLR ligands except flagellin enhanced Bet v 1 –allergen uptake 42. The gene discussed is TLR3; the disease is asthma.