We found that Gp2 expression was significantly increased in the pancreas of mice with colitis (Fig. 2c, d), indicating that an inflammatory signal (i.e., TNF) from the intestinal mucosa stimulates the pancreas to increase the expression of GP2 (Fig. 3d,e) and subsequently the amount of GP2 in the secretory granules (Fig. 3f) to prevent excess inflammation caused by bacterial stimulation. The gene discussed is TNF; the disease is colitis.