Although loss of Myd88 does not render humans susceptible to fungal infection (von Bernuth et al., 2008), studies have suggested that different human TLRs are able to activate specific arms of the antifungal defence, mainly in collaboration with dectin 1, while polymorphisms in several TLRs, including TLR1, TLR2, TLR3, TLR4, TLR6 and TLR9, have been associated with increased risk of fungal infections in immunocompromised individuals (reviewed by Cunha et al., 2010). This evidence concerns the gene CLEC7A and fungal infectious disease.