SHH and fibrosis: The expression of Shh/GLI activity was also significantly increased in the pancreas of caerulein induced chronic pancreatitis mice, and sulindac treatment showed a markedly down regulation of Shh and GLI1 mRNA and protein expression, implying that targeting Shh/GLI pathway by sulindac could be a mechanism for inhibiting pancreatic fibrosis and desmoplasia in chronic pancreatitis.