This lack of generalised immunosuppression has presumably arisen over the millennia of host-parasite evolution, generating a “safe” mechanism of immunomodulation tailored to specific aberrant inflammatory contexts and suggesting that the partial downregulation of MyD88 selectively targets certain regulatory nodes of the TLR4 (and other TLR) signalling cascades amplified in allergy and autoimmunity. This evidence concerns the gene TLR4 and allergic disease.