FXR-deficient mice were found to be more susceptible to indomethacin-induced gastric ulceration than their wild-type littermates, and the transfection of FXR into gastric adenocarcinoma cells protected against tumor necrosis factor α (TNFα)-induced cell damage, implying its gastroprotective activity in vitro and in vivo [115]. Here, TNF is linked to gastric ulcer.