These results collectively revealed that the CAPPZ2-induced tumor inhibition may be through promotion of apoptosis, which is in line with the activation of cytochrome-c, PARP, cleaved caspase-3 and Bax, as well as downregulation of Bcl-2 and ki67 in the CAPPZ2-treated tumor samples. The gene discussed is CASP3; the disease is neoplasm.