Alternatively, studies in mice have revealed that dysbiotic fecal microbiota from a genetically susceptible (e.g., Nod2 or Asc deficient) host can be dominantly transferred to healthy, wild-type recipients and is sufficient to increase sensitivity to DSS-induced colitis and tumorigenesis (Couturier-Maillard et al., 2013; Levy et al., 2015), indicating that dysbiotic communities have the capacity to increase disease risk in wild-type recipients via molecular signaling (e.g., cytokine modulation) under these experimental conditions. This evidence concerns the gene NOD2 and colitis.