In addition to MDSCs accumulation, the deletion of CARD9 or Syk also increases susceptibility to colitis and CAC in mouse model because of another protective mechanism, microbiota/Syk/CARD9/IL-18 axis, where commensal fungi promote the activation of inflammasome and the maturation of IL-18 in a CARD9-dependent manner to influence the restitution and maintenance of intestinal epithelial barrier and the production of IFN-γ (211). The gene discussed is SYK; the disease is colitis.