In addition to inhibiting tumor development from the ‘source of proliferation’, CO can further block cancer cell survival by regulating apoptosis-related pathways — specifically, it can induce apoptosis through two key mechanisms: It can also promote cell apoptosis by activating the Mitogen-Activated Protein Kinase (MAPK)/Extracellular Signal-Regulated Kinase 1/2 (Erk1/2) pathway and regulating B-cell lymphoma 2 (Bcl-2) family proteins [11,12]. This evidence concerns the gene MAPK3 and neoplasm.