At later time points than the 14 days assessed here it has been shown that the mice that survive completely clear the remaining Candida. The ultimate pathways responsible for the increased susceptibility of Dectin-2−/− mice to systemic candidiasis is most likely due to the combination of defective cytokine production, reduced neutrophil recruitment, and impaired phagocytosis of the fungus. The gene discussed is CLEC6A; the disease is candidiasis.