After supplementing with an opportunistic pathogen Candida tropicalis, Dectin-1-deficient mice exhibited more aggravated colitis and increased pro-inflammatory molecules (such as IFN-γ, IL-17, IL-23p19, TNF-α) in contrast to wild-type mice, but supplementing with nonpathogenic fungus Saccharomycopsis fibuligera did not contribute to mouse colitis (87). The gene discussed is IL23A; the disease is colitis.