In other cancers, CTSE has been shown to exert an antitumorigenic effect in prostate cancer cells—for example, by acting as the cleavage enzyme for tumor necrosis factor-related apoptosis ligand (TRAIL), which has also been implicated in the pathogenesis of EAC.29,30 Injection of purified CTSE into human tumor xenografts results in a dose-dependent induction of apoptosis and inhibition of tumor growth.29 It can therefore be speculated that the increased levels of CTSE in BE and BE/D may serve a protective mechanism. The gene discussed is CTSE; the disease is cancer.