Recently, Hsu et al. confirmed the importance of Dectin-1 in humans by demonstrating that a mutation in Clec7a that eliminates the C terminal β-glucan binding site was more prevalent in patients with disseminated coccidioidomycosis than in the general population, and that their monocyte-derived macrophages did not make TNFα when stimulated with curdlan (a Dectin-1 agonist) (see Section 2.6) [13]. The gene discussed is CLEC7A; the disease is coccidioidomycosis.