In animal model, we found that LXN deficiency leads to severity of DSS colitis, which can be demonstrated by a number of clinicopathological indicators, including more severe weight loss, hematochezia, shortening of the colon and rectum, damage to the mucosa and loss of goblet cells, increased proinflammatory cytokines and increased STAT3 activity. The gene discussed is STAT3; the disease is Hematochezia.