CAP increased the percentage of apoptotic tumor cells by blocking the cell cycle at the G2/M checkpoint, and this effect was mediated by reduced intracellular cyclin B1 and cyclin-dependent kinase 1 (Cdc2), increased p53 and cyclin-dependent kinase inhibitor 1 (p21), and increased Bcl-2-like protein 4 (Bax)/B cell lymphoma 2 (Bcl-2) ratio [111]. The gene discussed is CDKN1A; the disease is neoplasm.