They also showed that if Fas-mediated apoptosis in Jurkat cells is executed in the presence of mitochondria-specific inhibitors or synthetic caspase inhibitors, tumor-induced apoptosis is inhibited, suggesting that this phenomenon is significantly amplified by a mitochondrial loop and that tumor cells can trigger caspase-dependent apoptotic cascades in T lymphocytes [104, 105]. The gene discussed is FAS; the disease is neoplasm.