In humans, CLRs (for example, dectin-1, dectin-2, and the macrophage inducible Ca 2+-dependent lectin receptor MINCLE) that can recognise fungal pathogen-associated molecular patterns (PAMPs) and their adaptor molecule CARD9 have a critical role in antifungal host defence, and several studies highlighted an enhanced fungus-specific infection susceptibility as a consequence of mutations or deletions in CLRs or CARD9 [30,31]. The gene discussed is LARS1; the disease is infection.