Furthermore, we observed that ESC-2 resulted in apoptosis, activation of caspase-8 and caspase-3, and an increase in Fas expression, indicating that the NCI-H157 cell growth inhibitory activity of ESC-2 was due to death receptor-dependent pathway-mediated apoptosis, which may partly explain the anti-cancer activity of ESC-2. The gene discussed is CASP3; the disease is cancer.