Furthermore, Pan et al. revealed a different synthetic lethal therapy between p53 and B-cell lymphoma 2 (BCL-2) by activating p53 through MDM2 silencing and inhibiting BCL-2, which accelerates the apoptosis process in acute myeloid leukemia (AML) cells.59 This indicates that a combination of targeting mutated genes with their synthetic lethal partners may improve the synthetic lethal effects in more cancers than only inhibiting partner genes as in previous studies. The gene discussed is TP53; the disease is acute myeloid leukemia.