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Active inflammatory bowel disease (IBD) is often associated with simultaneous inflammation in the skin, eyes and joints. Inflammatory disease in the liver can also occur in patients with IBD but seems to be independent of inflammation in the bowel. In this Opinion article, we propose that the hepatic complications of IBD are mediated by long-lived mucosal T cells that are recruited to the liver in response to aberrantly expressed endothelial-cell adhesion molecules and chemokines that are normally restricted to the gut. Similar mechanisms might explain why certain diseases are associated with site-specific tissue distributions and might point to new therapeutic strategies that are based on modulating tissue-specific lymphocyte homing.