Although fat body antimicrobial peptide production may only be a generic defense response to the cuticle wound caused by the wasp ovipositor, or a byproduct of humoral activation of the Toll pathway for other reasons, and not an immune response to the parasite itself [5,91], it is striking that Lh14 infection appears to result in the specific suppression of fat body activation of the Drosomycin promoter, a well-characterized downstream effector of the Toll pathway [92]. This evidence concerns the gene TLR4 and infection.