CP caused apoptosis through simultaneously inhibiting Akt/mammalian target of rapamycin (mTOR) while exciting Jun N-terminal kinase (JNK) and p38 MAPK signalling pathways, leading to autophagy and the activation of p53-mediated activation of proapoptotic caspases, while inactivating Akt also inhibited NFκB to reduce tumour cell proliferation [163,164]. The gene discussed is TP53; the disease is neoplasm.