The discovery in 1996 that the Drosophila transmembrane protein Toll specifically mediates the recognition and the response to fungal infection [6], followed by the cloning of several related receptors in other species, including human [7] and the discovery that one of these molecules (TLR4) is the receptor for lipopolysaccharide (LPS) [8], challenged the dogma that attributed nonspecificity to innate immunity. The gene discussed is TLR4; the disease is fungal infectious disease.