A similar study further showed that the inhibition of FXR in esophageal adenocarcinoma tissues either with an expression of FXR shRNA or treatment with GS suppressed tumor cell viability and induced apoptosis in vitro and in vivo [16] suggesting GS as a potential antagonist to FXR overexpression and a cancer chemotherapeutic. Here, NR1H4 is linked to esophageal adenocarcinoma.