Upon administration with AOM-DSS, CARD9-null mice are proven to be more susceptible to CAC, whose mechanism is that defective fungicidal functions of Card9-null macrophages lead to fungal dysbiosis (especially increased Candida tropicalis), and C. tropicalis increases the number of intestinal MDSC and activates the function of MDSC (206). This evidence concerns the gene CARD9 and infectious otitis media.