In general, in mouse models of colitis where the epithelial barrier is severely disrupted due to chemical compounds or genetic defects, such as in the DSS-colitis model (28, 29), N-cadherin dominant negative mice (30), Muc1/2−/− mice (31, 32), Mdr1a−/− mice (33), or in those animals where the immune response is compromised due to the genetic background, such as in IL10−/− and Stat3−/− mice (34, 35), inflammation is absent when animals are maintained under germ-free conditions. The gene discussed is STAT3; the disease is colitis.