BCL2 and acute myeloid leukemia: 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.